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dict |
|---|---|---|---|---|---|---|---|---|---|---|
10945637.s12 | Thus, FGF6 is increased in PIN and prostate cancer and can promote the proliferation of the transformed prostatic epithelial cells via paracrine and autocrine mechanisms. | prostate | {
"name": "FGF6",
"pos": [
6,
9
]
} | {
"name": "prostate cancer",
"pos": [
35,
49
]
} | increased | normalTOcancer | causality | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increased",
"pos": [
14,
22
],
"type": "Positive_regulation"
} |
11722842.s0 | Isolation and characterization of the major form of human MUC18 cDNA gene and correlation of MUC18 over-expression in prostate cancer cell lines and tissues with malignant progression. | prostate | {
"name": "MUC18",
"pos": [
93,
97
]
} | {
"name": "prostate cancer",
"pos": [
118,
132
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "over-expression",
"pos": [
99,
113
],
"type": "Gene_expression"
} | {
"name": "over-expression",
"pos": [
99,
113
],
"type": "Positive_regulation"
} |
11722842.s13 | We therefore conclude that MUC18 expression is increased during prostate cancer initiation (high grade PIN) and progression to carcinoma, and in metastatic cell lines and metastatic carcinoma. | prostate | {
"name": "MUC18",
"pos": [
27,
31
]
} | {
"name": "prostate cancer",
"pos": [
64,
78
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
33,
42
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
47,
55
],
"type": "Positive_regulation"
} |
11839683.s9 | These results demonstrate that in a sequence-specific manner, RIalpha antisense, via efficient depletion of the growth stimulatory molecule RIalpha, induces growth inhibition, apoptosis, and phenotypic (cell morphology) changes, providing an innovative approach to combat hormone-insensitive prostate cancer cell growth. | prostate | {
"name": "growth stimulatory molecule RIalpha",
"pos": [
112,
146
]
} | {
"name": "prostate cancer",
"pos": [
292,
306
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "depletion",
"pos": [
95,
103
],
"type": "Negative_regulation"
} |
12006585.s2 | We have found that Cdc6 expression is down-regulated in prostate cancer as detected by semiquantitative reverse transcriptase-PCR of prostate cell lines and laser-captured microdissected prostate tissues. | prostate | {
"name": "Cdc6",
"pos": [
19,
22
]
} | {
"name": "prostate cancer",
"pos": [
56,
70
]
} | decreased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
24,
33
],
"type": "Gene_expression"
} | {
"name": "down-regulated",
"pos": [
38,
51
],
"type": "Negative_regulation"
} |
12006585.s4 | Furthermore, a 100-fold reduction in the transcription efficiency of the Cdc6 promoter-luciferase construct was noted in the metastatic PC3 cells compared with that in BPH-1 cells. | prostate | {
"name": "Cdc6 promoter-luciferase construct",
"pos": [
73,
106
]
} | {
"name": "PC3",
"pos": [
136,
138
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "reduction",
"pos": [
24,
32
],
"type": "Negative_regulation"
} |
12409226.s7 | Sustained increase of the c-myc gene product was detectable in PC-3 but not in DU-145 cells. | prostate | {
"name": "c-myc gene product",
"pos": [
26,
43
]
} | {
"name": "PC-3",
"pos": [
63,
66
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increase",
"pos": [
10,
17
],
"type": "Positive_regulation"
} |
12409226.s8 | Concurrently, we demonstrated BN-dependent activation of the transcription factor Elk-1 and significant increase of cell proliferation in both prostate cancer cell lines. | prostate | {
"name": "transcription factor Elk-1",
"pos": [
61,
86
]
} | {
"name": "prostate cancer",
"pos": [
143,
157
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
43,
52
],
"type": "Positive_regulation"
} |
12433721.s1 | Electronic profiling of publicly available expressed sequence tag databases identified a gene, cysteine-rich secretoryprotein-3 (CRISP-3), that is up-regulated in prostate cancer, and of which the expression is relatively prostate-specific. | prostate | {
"name": "CRISP-3",
"pos": [
129,
135
]
} | {
"name": "prostate cancer",
"pos": [
163,
177
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "up-regulated",
"pos": [
147,
158
],
"type": "Positive_regulation"
} |
12569365.s4 | Cdc25B is frequently overexpressed in human prostate cancer tissues (29 of 30; 97%). | prostate | {
"name": "Cdc25B",
"pos": [
0,
5
]
} | {
"name": "prostate cancer",
"pos": [
44,
58
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpressed",
"pos": [
21,
33
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
21,
33
],
"type": "Positive_regulation"
} |
12598323.s1 | PTOV1 was recently identified as a novel gene and protein during a differential display screening for genes overexpressed in prostate cancer. | prostate | {
"name": "PTOV1",
"pos": [
0,
4
]
} | {
"name": "prostate cancer",
"pos": [
125,
139
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpressed",
"pos": [
108,
120
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
108,
120
],
"type": "Positive_regulation"
} |
12598323.s3 | By immunohistochemical analysis, we have found that PTOV1 is overexpressed in 71% of 38 prostate carcinomas and in 80% of samples with prostate intraepithelial neoplasia. | prostate | {
"name": "PTOV1",
"pos": [
52,
56
]
} | {
"name": "prostate carcinomas",
"pos": [
88,
106
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpressed",
"pos": [
61,
73
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
61,
73
],
"type": "Positive_regulation"
} |
12618764.s0 | MEK5 overexpression is associated with metastatic prostate cancer, and stimulates proliferation, MMP-9 expression and invasion. | prostate | {
"name": "MEK5",
"pos": [
0,
3
]
} | {
"name": "prostate cancer",
"pos": [
50,
64
]
} | increased | normalTOcancer | causality | unchanged | {
"name": "overexpression",
"pos": [
5,
18
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
5,
18
],
"type": "Positive_regulation"
} |
12875974.s2 | The overexpression of Bax inhibitor-1 (BI-1) in prostate carcinoma and prostate cancer cell lines was confirmed by using Northern blot and Western blot analyses. | prostate | {
"name": "BI-1",
"pos": [
39,
42
]
} | {
"name": "prostate cancer",
"pos": [
71,
85
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpression",
"pos": [
4,
17
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
4,
17
],
"type": "Positive_regulation"
} |
12907652.s9 | These observations suggest that U19 is growth inhibitory and tumor suppressive and that the disruption of androgen-dependent growth inhibition via U19 down-regulation is commonly associated with prostate cancer progression. | prostate | {
"name": "U19",
"pos": [
147,
149
]
} | {
"name": "prostate cancer",
"pos": [
195,
209
]
} | decreased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "down-regulation",
"pos": [
151,
165
],
"type": "Negative_regulation"
} |
14744752.s5 | First, a comprehensive serial immunohistochemical analysis of primary and metastatic prostate cancer samples showed increased stage-specific expression of IL-11Ralpha during disease progression. | prostate | {
"name": "IL-11Ralpha",
"pos": [
155,
165
]
} | {
"name": "prostate cancer",
"pos": [
85,
99
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
141,
150
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
116,
124
],
"type": "Positive_regulation"
} |
14744778.s2 | We have shown previously that although AP-2 is expressed highly in normal prostatic epithelium, its expression is lost in high-grade prostatic intraepithelial neoplasia and prostate cancer, suggesting that loss of AP-2 plays a role in prostate cancer development. | prostate | {
"name": "AP-2",
"pos": [
214,
217
]
} | {
"name": "prostate cancer",
"pos": [
173,
187
]
} | decreased | normalTOcancer | causality | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "loss",
"pos": [
206,
209
],
"type": "Negative_regulation"
} |
14744778.s10 | Elucidating the molecular events resulting from loss of AP-2 in the prostate epithelium has implications for the understanding and prevention of the onset of prostate cancer. | prostate | {
"name": "AP-2",
"pos": [
56,
59
]
} | {
"name": "prostate cancer",
"pos": [
158,
172
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "loss",
"pos": [
48,
51
],
"type": "Negative_regulation"
} |
||
14766760.s7 | The interaction between FADD and caspase-8 was inhibited, but abrogation of JNK activity or HIPK3 expression was found to restore this interaction and increased the sensitivity of DU 145 cells to Fas receptor-mediated apoptosis. | prostate | {
"name": "HIPK3",
"pos": [
92,
96
]
} | {
"name": "DU 145",
"pos": [
180,
185
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "expression",
"pos": [
98,
107
],
"type": "Gene_expression"
} | {
"name": "abrogation",
"pos": [
62,
71
],
"type": "Negative_regulation"
} |
15026365.s14 | In clinical prostate cancer specimens from patients with varying grades of disease, the stained tissue sections showed high levels of SREBP-1 protein compared with noncancerous prostate tissue. | prostate | {
"name": "SREBP-1 protein",
"pos": [
134,
148
]
} | {
"name": "prostate cancer",
"pos": [
12,
26
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "levels",
"pos": [
124,
129
],
"type": "Positive_regulation"
} |
15026365.s17 | In summary, the LNCaP xenograft model of human prostate cancer as well as clinical specimens of prostate cancer demonstrated an up-regulation of SREBPs and their downstream effector genes during progression to androgen independence. | prostate | {
"name": "SREBPs",
"pos": [
145,
150
]
} | {
"name": "prostate cancer",
"pos": [
47,
61
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "up-regulation",
"pos": [
128,
140
],
"type": "Positive_regulation"
} |
15833840.s1 | An increase in the activity of mitogen-activated protein kinase (MAPK) has been correlated with the progression of prostate cancer to advanced disease in humans. | prostate | {
"name": "mitogen-activated protein kinase",
"pos": [
31,
62
]
} | {
"name": "prostate cancer",
"pos": [
115,
129
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increase",
"pos": [
3,
10
],
"type": "Positive_regulation"
} |
15833840.s3 | Increasing RSK isoform 2 (RSK2) levels in the human prostate cancer line, LNCaP, enhanced prostate-specific antigen (PSA) expression, an important diagnostic marker for prostate cancer, whereas inhibiting RSK activity using a RSK-specific inhibitor, 3Ac-SL0101, decreased PSA expression. | prostate | {
"name": "PSA",
"pos": [
117,
119
]
} | {
"name": "prostate cancer",
"pos": [
52,
66
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
122,
131
],
"type": "Gene_expression"
} | {
"name": "enhanced",
"pos": [
81,
88
],
"type": "Positive_regulation"
} |
15833840.s3 | Increasing RSK isoform 2 (RSK2) levels in the human prostate cancer line, LNCaP, enhanced prostate-specific antigen (PSA) expression, an important diagnostic marker for prostate cancer, whereas inhibiting RSK activity using a RSK-specific inhibitor, 3Ac-SL0101, decreased PSA expression. | prostate | {
"name": "PSA",
"pos": [
272,
274
]
} | {
"name": "prostate cancer",
"pos": [
52,
66
]
} | decreased | unidentifiable | {
"name": "expression",
"pos": [
276,
285
],
"type": "Gene_expression"
} | {
"name": "decreased",
"pos": [
262,
270
],
"type": "Negative_regulation"
} |
||
15837784.s0 | Down-regulation of ATM protein sensitizes human prostate cancer cells to radiation-induced apoptosis. | prostate | {
"name": "ATM protein",
"pos": [
19,
29
]
} | {
"name": "prostate cancer",
"pos": [
48,
62
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Down-regulation",
"pos": [
0,
14
],
"type": "Negative_regulation"
} |
15897876.s7 | CBX7 overexpression in LNCaP cells resulted in a slight growth advantage in both androgen-dependent and -independent conditions. | prostate | {
"name": "CBX7",
"pos": [
0,
3
]
} | {
"name": "LNCaP",
"pos": [
23,
27
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "overexpression",
"pos": [
5,
18
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
5,
18
],
"type": "Positive_regulation"
} |
16115918.s1 | Cytochrome P450 1B1 (CYP1B1), a dioxin inducible member of the CYP supergene family, is overexpressed in various human malignancies including prostate cancer. | prostate | {
"name": "Cytochrome P450 1B1 (CYP1B1)",
"pos": [
0,
27
]
} | {
"name": "prostate cancer",
"pos": [
142,
156
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpressed",
"pos": [
88,
100
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
88,
100
],
"type": "Positive_regulation"
} |
16424021.s0 | Increased expression of osteopontin contributes to the progression of prostate cancer. | prostate | {
"name": "osteopontin",
"pos": [
24,
34
]
} | {
"name": "prostate cancer",
"pos": [
70,
84
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "expression",
"pos": [
10,
19
],
"type": "Gene_expression"
} | {
"name": "Increased",
"pos": [
0,
8
],
"type": "Positive_regulation"
} |
16601286.s0 | Increased expression of type 2 3alpha-hydroxysteroid dehydrogenase/type 5 17beta-hydroxysteroid dehydrogenase (AKR1C3) and its relationship with androgen receptor in prostate carcinoma. | prostate | {
"name": "type 2 3alpha-hydroxysteroid dehydrogenase/type 5 17beta-hydroxysteroid dehydrogenase (AKR1C3)",
"pos": [
24,
117
]
} | {
"name": "prostate carcinoma",
"pos": [
166,
183
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
10,
19
],
"type": "Gene_expression"
} | {
"name": "Increased",
"pos": [
0,
8
],
"type": "Positive_regulation"
} |
||
16601286.s13 | We conclude that elevated expression of AKR1C3 is highly associated with prostate carcinoma. | prostate | {
"name": "AKR1C3",
"pos": [
40,
45
]
} | {
"name": "prostate carcinoma",
"pos": [
73,
90
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
26,
35
],
"type": "Gene_expression"
} | {
"name": "elevated",
"pos": [
17,
24
],
"type": "Positive_regulation"
} |
16609016.s9 | Kaplan-Meier survival analysis confirmed increased RPL19 expression to be highly predictive of shorter patient survival (P < 0.05), revealing RPL19 to be a sensitive predictor of prostate cancer progression. | prostate | {
"name": "RPL19",
"pos": [
51,
55
]
} | {
"name": "prostate cancer",
"pos": [
182,
196
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
57,
66
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
41,
49
],
"type": "Positive_regulation"
} |
||
16818616.s6 | Transfection-mediated WWOX overexpression in DU145 cells suppressed colony growth (P = 0.0012), and WWOX overexpression by infection with Ad-WWOX virus induced apoptosis through a caspase-dependent mechanism and suppressed cell growth. | prostate | {
"name": "WWOX",
"pos": [
100,
103
]
} | {
"name": "DU145",
"pos": [
45,
49
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "overexpression",
"pos": [
105,
118
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
105,
118
],
"type": "Positive_regulation"
} |
17003780.s7 | Together, our data suggest that strong Tiam1 overexpression relative to the corresponding benign epithelial cells is a new and independent predictor of decreased DFS for patients with prostate cancer. | prostate | {
"name": "Tiam1",
"pos": [
39,
43
]
} | {
"name": "prostate cancer",
"pos": [
184,
198
]
} | increased | unidentifiable | {
"name": "overexpression",
"pos": [
45,
58
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
45,
58
],
"type": "Positive_regulation"
} |
||
17134822.s0 | Polycomb-group oncogenes EZH2, BMI1, and RING1 are overexpressed in prostate cancer with adverse pathologic and clinical features. | prostate | {
"name": "Polycomb-group oncogenes EZH2",
"pos": [
0,
28
]
} | {
"name": "prostate cancer",
"pos": [
68,
82
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpressed",
"pos": [
51,
63
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
51,
63
],
"type": "Positive_regulation"
} |
17481580.s4 | Out of seven isoforms of gal8, the proto isoform gal8e and our newly discovered proto isoform gal8g were upregulated in LNCaP cells compared to PrEC, whereas the two tandem-repeat isoforms gal8a and gal8b were equally expressed in these cells. | prostate | {
"name": "gal8e",
"pos": [
49,
53
]
} | {
"name": "LNCaP",
"pos": [
120,
124
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "upregulated",
"pos": [
105,
115
],
"type": "Positive_regulation"
} |
17481580.s4 | Out of seven isoforms of gal8, the proto isoform gal8e and our newly discovered proto isoform gal8g were upregulated in LNCaP cells compared to PrEC, whereas the two tandem-repeat isoforms gal8a and gal8b were equally expressed in these cells. | prostate | {
"name": "gal8g",
"pos": [
94,
98
]
} | {
"name": "LNCaP",
"pos": [
120,
124
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "upregulated",
"pos": [
105,
115
],
"type": "Positive_regulation"
} |
17513602.s0 | Increased expression of cyclin B1 sensitizes prostate cancer cells to apoptosis induced by chemotherapy. | prostate | {
"name": "cyclin B1",
"pos": [
24,
32
]
} | {
"name": "prostate cancer",
"pos": [
45,
59
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "expression",
"pos": [
10,
19
],
"type": "Gene_expression"
} | {
"name": "Increased",
"pos": [
0,
8
],
"type": "Positive_regulation"
} |
17875724.s7 | We present here for the first time that signal transducers and activators of transcription 3 (Stat3), which is constitutively activated in a wide variety of human cancers, including prostate cancer, interacts with PKCepsilon. | prostate | {
"name": "signal transducers and activators of transcription 3",
"pos": [
40,
91
]
} | {
"name": "prostate cancer",
"pos": [
182,
196
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activated",
"pos": [
126,
134
],
"type": "Positive_regulation"
} |
17908958.s0 | Smad3 is overexpressed in advanced human prostate cancer and necessary for progressive growth of prostate cancer cells in nude mice. | prostate | {
"name": "Smad3",
"pos": [
0,
4
]
} | {
"name": "prostate cancer",
"pos": [
41,
55
]
} | increased | normalTOcancer | causality | unchanged | {
"name": "overexpressed",
"pos": [
9,
21
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
9,
21
],
"type": "Positive_regulation"
} |
18008330.s1 | Clinical data showed that the levels of interleukin-4 (IL-4) are significantly elevated in serum of patients with ablation resistant prostate cancer. | prostate | {
"name": "interleukin-4",
"pos": [
40,
52
]
} | {
"name": "prostate cancer",
"pos": [
133,
147
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "levels",
"pos": [
30,
35
],
"type": "Gene_expression"
} | {
"name": "elevated",
"pos": [
79,
86
],
"type": "Positive_regulation"
} |
18008330.s9 | Overexpression of IL-4 increases the sensitivity of androgen-sensitive LNCaP prostate cancer cells in response to androgen stimulation and enhances the growth of LNCaP cells both in the presence and absence of androgen in vitro and in vivo. | prostate | {
"name": "IL-4",
"pos": [
18,
21
]
} | {
"name": "prostate cancer",
"pos": [
77,
91
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Gene_expression"
} | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Positive_regulation"
} |
18167127.s0 | Loss of BRCA2 promotes prostate cancer cell invasion through up-regulation of matrix metalloproteinase-9. | prostate | {
"name": "BRCA2",
"pos": [
8,
12
]
} | {
"name": "prostate cancer",
"pos": [
23,
37
]
} | decreased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Loss",
"pos": [
0,
3
],
"type": "Negative_regulation"
} |
18167127.s6 | Consistently, PI3-kinase inhibition with a dominant-negative mutant or MAPK/ERK activation with a gain-of-function mutant reduced MMP-9 levels and prevented migration and invasion in wild-type PC-3 cells. | prostate | {
"name": "PI3-kinase",
"pos": [
14,
23
]
} | {
"name": "PC-3",
"pos": [
193,
196
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibition",
"pos": [
25,
34
],
"type": "Negative_regulation"
} |
11431361.s0 | Hyaluronan synthase 3 overexpression promotes the growth of TSU prostate cancer cells. | prostate | {
"name": "Hyaluronan synthase 3",
"pos": [
0,
20
]
} | {
"name": "prostate cancer",
"pos": [
64,
78
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "overexpression",
"pos": [
22,
35
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
22,
35
],
"type": "Positive_regulation"
} |
16491480.s2 | We have previously described the increased expression of two prostate-specific G-protein coupled receptors (PSGR and PSGR2) in human prostate cancer. | prostate | {
"name": "PSGR",
"pos": [
108,
111
]
} | {
"name": "prostate cancer",
"pos": [
133,
147
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
43,
52
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
33,
41
],
"type": "Positive_regulation"
} |
16491480.s2 | We have previously described the increased expression of two prostate-specific G-protein coupled receptors (PSGR and PSGR2) in human prostate cancer. | prostate | {
"name": "PSGR2",
"pos": [
117,
121
]
} | {
"name": "prostate cancer",
"pos": [
133,
147
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
43,
52
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
33,
41
],
"type": "Positive_regulation"
} |
16491480.s9 | AMACR was the best single marker of prostate cancer but in 7 of the 59 total cases the expression of AMACR was not significantly elevated while PSGR and/or PSGR2 were substantially elevated. | prostate | {
"name": "PSGR",
"pos": [
144,
147
]
} | {
"name": "prostate cancer",
"pos": [
36,
50
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "elevated",
"pos": [
181,
188
],
"type": "Positive_regulation"
} |
17426117.s3 | Reduction of AR expression in the two androgen-sensitive prostate cancer cell lines, LNCaP and LAPC4, significantly decreased AR-mediated transcription and cell growth. | prostate | {
"name": "AR",
"pos": [
13,
14
]
} | {
"name": "prostate cancer",
"pos": [
57,
71
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "expression",
"pos": [
16,
25
],
"type": "Gene_expression"
} | {
"name": "Reduction",
"pos": [
0,
8
],
"type": "Negative_regulation"
} |
8612685.s0 | Downregulation of protein kinase C suppresses induction of apoptosis in human prostatic carcinoma cells. | prostate | {
"name": "protein kinase C",
"pos": [
18,
33
]
} | {
"name": "prostatic carcinoma",
"pos": [
78,
96
]
} | decreased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Downregulation",
"pos": [
0,
13
],
"type": "Negative_regulation"
} |
8612685.s7 | PKC isozyme analysis revealed that chronic PDBu treatment caused downregulation of PKC-alpha and -epsilon in DU-145 cells. | prostate | {
"name": "PKC-alpha and -epsilon",
"pos": [
83,
104
]
} | {
"name": "DU-145",
"pos": [
109,
114
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "downregulation",
"pos": [
65,
78
],
"type": "Negative_regulation"
} |
||
12544353.s7 | Antisense bcl-2 oligodeoxynucleotides decreased Bcl-2 protein levels and significantly inhibited PC-3 cell growth in a dose dependent manner. | prostate | {
"name": "Bcl-2 protein",
"pos": [
48,
60
]
} | {
"name": "PC-3",
"pos": [
97,
100
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "decreased",
"pos": [
38,
46
],
"type": "Negative_regulation"
} |
16302272.s1 | Experimental work in various prostate cancer models revealed that the androgen receptor is frequently upregulated and implicated in tumor progression. | prostate | {
"name": "androgen receptor",
"pos": [
70,
86
]
} | {
"name": "prostate cancer",
"pos": [
29,
43
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "upregulated",
"pos": [
102,
112
],
"type": "Positive_regulation"
} |
21320357.s4 | EPCR expression is up-regulated both at the mRNA and protein levels in invasive prostate DU-145 and PC-3 cells in comparison to normal prostate epithelial cells (PrEC) and less-invasive LNCaP cells. | prostate | {
"name": "EPCR",
"pos": [
0,
3
]
} | {
"name": "DU-145",
"pos": [
89,
94
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
5,
14
],
"type": "Gene_expression"
} | {
"name": "up-regulated",
"pos": [
19,
30
],
"type": "Positive_regulation"
} |
15638997.s4 | Response to bicalutamide in LNCaP cells was represented by downregulation of androgen-regulated genes, activation of the p53 pathway and inhibition of telomerase, which was associated with downregulation of v-myc avian myelocytomatosis viral oncogene homologue (MYC) and telomerase reverse transcriptase subunit. | prostate | {
"name": "p53",
"pos": [
121,
123
]
} | {
"name": "LNCaP",
"pos": [
28,
32
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
103,
112
],
"type": "Positive_regulation"
} |
||
15638997.s4 | Response to bicalutamide in LNCaP cells was represented by downregulation of androgen-regulated genes, activation of the p53 pathway and inhibition of telomerase, which was associated with downregulation of v-myc avian myelocytomatosis viral oncogene homologue (MYC) and telomerase reverse transcriptase subunit. | prostate | {
"name": "MYC",
"pos": [
262,
264
]
} | {
"name": "LNCaP",
"pos": [
28,
32
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "downregulation",
"pos": [
189,
202
],
"type": "Negative_regulation"
} |
||
15638997.s4 | Response to bicalutamide in LNCaP cells was represented by downregulation of androgen-regulated genes, activation of the p53 pathway and inhibition of telomerase, which was associated with downregulation of v-myc avian myelocytomatosis viral oncogene homologue (MYC) and telomerase reverse transcriptase subunit. | prostate | {
"name": "telomerase reverse transcriptase subunit",
"pos": [
271,
310
]
} | {
"name": "LNCaP",
"pos": [
28,
32
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "downregulation",
"pos": [
189,
202
],
"type": "Negative_regulation"
} |
||
15638997.s6 | In conclusion, we provide an explanation for telomerase inhibition after androgen receptor blockade in LNCaP cells and we also report activation of the p53 pathway in LNCaP cells and in-vitro sensitivity to bicalutamide of low confluent androgen-insensitive DU145 cells. | prostate | {
"name": "p53",
"pos": [
152,
154
]
} | {
"name": "LNCaP",
"pos": [
103,
107
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
134,
143
],
"type": "Positive_regulation"
} |
15638997.s6 | In conclusion, we provide an explanation for telomerase inhibition after androgen receptor blockade in LNCaP cells and we also report activation of the p53 pathway in LNCaP cells and in-vitro sensitivity to bicalutamide of low confluent androgen-insensitive DU145 cells. | prostate | {
"name": "androgen receptor",
"pos": [
73,
89
]
} | {
"name": "LNCaP",
"pos": [
103,
107
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "blockade",
"pos": [
91,
98
],
"type": "Negative_regulation"
} |
||
19584279.s0 | Reactivation of androgen receptor-regulated TMPRSS2:ERG gene expression in castration-resistant prostate cancer. | prostate | {
"name": "androgen receptor-regulated TMPRSS2",
"pos": [
16,
50
]
} | {
"name": "prostate cancer",
"pos": [
96,
110
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Reactivation",
"pos": [
0,
11
],
"type": "Positive_regulation"
} |
19584279.s0 | Reactivation of androgen receptor-regulated TMPRSS2:ERG gene expression in castration-resistant prostate cancer. | prostate | {
"name": "ERG gene",
"pos": [
52,
59
]
} | {
"name": "prostate cancer",
"pos": [
96,
110
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
61,
70
],
"type": "Gene_expression"
} | {
"name": "Reactivation",
"pos": [
0,
11
],
"type": "Positive_regulation"
} |
19584279.s5 | Moreover, as observed in the clinical samples, ERG expression was fully restored in the VCaP xenografts that relapsed after castration, coincident with AR reactivation. | prostate | {
"name": "ERG",
"pos": [
47,
49
]
} | {
"name": "VCaP",
"pos": [
88,
91
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
51,
60
],
"type": "Gene_expression"
} | {
"name": "restored",
"pos": [
72,
79
],
"type": "Positive_regulation"
} |
19584279.s5 | Moreover, as observed in the clinical samples, ERG expression was fully restored in the VCaP xenografts that relapsed after castration, coincident with AR reactivation. | prostate | {
"name": "AR",
"pos": [
152,
153
]
} | {
"name": "VCaP",
"pos": [
88,
91
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "reactivation",
"pos": [
155,
166
],
"type": "Positive_regulation"
} |
18358509.s4 | We observed that re-expression of AR in the AR-negative cells PC3 decreases anchorage-independent growth and Matrigel invasiveness of PC3-AR cells where plasma membrane interaction between AR and EGFR led to an interference with downstream signalling and internalization of activated EGFR. | prostate | {
"name": "EGFR",
"pos": [
284,
287
]
} | {
"name": "PC3",
"pos": [
62,
64
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activated",
"pos": [
274,
282
],
"type": "Positive_regulation"
} |
||
16427044.s4 | M12 cells, like many other human cancer cells, contain constitutively activated signal transducer and activator of transcription 3 (STAT3). | prostate | {
"name": "STAT3",
"pos": [
132,
136
]
} | {
"name": "M12",
"pos": [
0,
2
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activated",
"pos": [
70,
78
],
"type": "Positive_regulation"
} |
16427044.s6 | Strikingly, IFN-gamma-induced apoptosis and growth inhibition of M12 cells were associated with persistent suppression of the constitutive tyrosine-phosphorylated STAT3 (pY-STAT3). | prostate | {
"name": "STAT3",
"pos": [
163,
167
]
} | {
"name": "M12",
"pos": [
65,
67
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "suppression",
"pos": [
107,
117
],
"type": "Negative_regulation"
} |
20336778.s3 | In this study, while demonstrating suppressed levels of Tm1 in the prostate cancer cell lines LNCaP, PC3, and DU-145 compared to normal prostate epithelial cell primary isolates (PrEC), a novel splice variant of the TPM2 gene was identified. | prostate | {
"name": "Tm1",
"pos": [
56,
58
]
} | {
"name": "prostate cancer",
"pos": [
67,
81
]
} | decreased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "suppressed",
"pos": [
35,
44
],
"type": "Negative_regulation"
} |
10931458.s14 | These findings suggest that inhibition of COX-2 development may lead not only to inhibition of the proliferation and metastasis of prostate carcinoma but also to the inhibition of prostate carcinogenesis. | prostate | {
"name": "COX-2",
"pos": [
42,
46
]
} | {
"name": "prostate carcinoma",
"pos": [
131,
148
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibition",
"pos": [
28,
37
],
"type": "Negative_regulation"
} |
18349265.s4 | Prostate cancer bony metastases show increased expression of the PTH receptor (PTH-IR) and PTH promotes the growth and invasiveness of prostate cancer cells in bone. | prostate | {
"name": "PTH receptor",
"pos": [
65,
76
]
} | {
"name": "prostate cancer",
"pos": [
135,
149
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "expression",
"pos": [
47,
56
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
37,
45
],
"type": "Positive_regulation"
} |
18349265.s4 | Prostate cancer bony metastases show increased expression of the PTH receptor (PTH-IR) and PTH promotes the growth and invasiveness of prostate cancer cells in bone. | prostate | {
"name": "PTH-IR",
"pos": [
79,
84
]
} | {
"name": "prostate cancer",
"pos": [
135,
149
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "expression",
"pos": [
47,
56
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
37,
45
],
"type": "Positive_regulation"
} |
18349265.s4 | Prostate cancer bony metastases show increased expression of the PTH receptor (PTH-IR) and PTH promotes the growth and invasiveness of prostate cancer cells in bone. | prostate | {
"name": "PTH",
"pos": [
91,
93
]
} | {
"name": "prostate cancer",
"pos": [
135,
149
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "expression",
"pos": [
47,
56
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
37,
45
],
"type": "Positive_regulation"
} |
10216950.s8 | A broad spectrum of tumor derived cell lines, from varied tissue sources and blood samples from patients having confirmed prostate carcinoma, all scored positive for expression of PTI-1, while corresponding normal tissues or blood samples were negative. | prostate | {
"name": "PTI-1",
"pos": [
180,
184
]
} | {
"name": "prostate carcinoma",
"pos": [
122,
139
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
166,
175
],
"type": "Gene_expression"
} | {
"name": "positive",
"pos": [
153,
160
],
"type": "Positive_regulation"
} |
9586898.s11 | A decrease in PSA level is associated with both survival and response in soft tissue lesions and should be incorporated into the response criteria and reporting of trials of cytotoxic agents in prostate cancer. | prostate | {
"name": "PSA",
"pos": [
14,
16
]
} | {
"name": "prostate cancer",
"pos": [
194,
208
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "decrease",
"pos": [
2,
9
],
"type": "Negative_regulation"
} |
||
21064106.s0 | miR 488* inhibits androgen receptor expression in prostate carcinoma cells. | prostate | {
"name": "androgen receptor",
"pos": [
18,
34
]
} | {
"name": "prostate carcinoma",
"pos": [
50,
67
]
} | decreased | unidentifiable | {
"name": "expression",
"pos": [
36,
45
],
"type": "Gene_expression"
} | {
"name": "inhibits",
"pos": [
9,
16
],
"type": "Negative_regulation"
} |
||
17409433.s3 | NSAIDs exert their anti-inflammatory effects by inhibiting cyclooxygenase (COX) activity; however, evidence suggests that COX-independent mechanisms mediate decreased prostate cancer cell survival. | prostate | {
"name": "cyclooxygenase",
"pos": [
59,
72
]
} | {
"name": "prostate cancer",
"pos": [
167,
181
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibiting",
"pos": [
48,
57
],
"type": "Negative_regulation"
} |
||
17409433.s3 | NSAIDs exert their anti-inflammatory effects by inhibiting cyclooxygenase (COX) activity; however, evidence suggests that COX-independent mechanisms mediate decreased prostate cancer cell survival. | prostate | {
"name": "COX",
"pos": [
75,
77
]
} | {
"name": "prostate cancer",
"pos": [
167,
181
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibiting",
"pos": [
48,
57
],
"type": "Negative_regulation"
} |
||
17409433.s10 | Hence, R-flurbiprofen and ibuprofen selectively induce p75(NTR)-dependent decreased survival of prostate cancer cells independently of COX inhibition. | prostate | {
"name": "COX",
"pos": [
135,
137
]
} | {
"name": "prostate cancer",
"pos": [
96,
110
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibition",
"pos": [
139,
148
],
"type": "Negative_regulation"
} |
||
11704864.s5 | Here we show that an increase in the level of expression of Bcl-2 in the human prostate carcinoma cell line LNCaP observed in response to hormone withdrawal is further augmented by TNF-alpha treatment, and this effect is abated by inhibitors of NF-kappa B. | prostate | {
"name": "NF-kappa B",
"pos": [
245,
254
]
} | {
"name": "prostate carcinoma",
"pos": [
79,
96
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibitors",
"pos": [
231,
240
],
"type": "Negative_regulation"
} |
||
11704864.s6 | Concomitantly, bcl-2 p2 promoter studies in LNCaP cells show a 40-fold increase in promoter activity after stimulation with TNF-alpha in the absence of hormone. | prostate | {
"name": "TNF-alpha",
"pos": [
124,
132
]
} | {
"name": "LNCaP",
"pos": [
44,
48
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "stimulation",
"pos": [
107,
117
],
"type": "Positive_regulation"
} |
||
11704864.s5 | Here we show that an increase in the level of expression of Bcl-2 in the human prostate carcinoma cell line LNCaP observed in response to hormone withdrawal is further augmented by TNF-alpha treatment, and this effect is abated by inhibitors of NF-kappa B. | prostate | {
"name": "Bcl-2",
"pos": [
60,
64
]
} | {
"name": "prostate carcinoma",
"pos": [
79,
96
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
46,
55
],
"type": "Gene_expression"
} | {
"name": "increase",
"pos": [
21,
28
],
"type": "Positive_regulation"
} |
||
19879420.s2 | For example, some studies showed that CLU expression is increased in advanced stages of prostate cancer and that suppression of CLU expression sensitizes prostate cancer cells to chemotherapeutic drugs killing. | prostate | {
"name": "CLU",
"pos": [
128,
130
]
} | {
"name": "prostate cancer",
"pos": [
88,
102
]
} | decreased | cancerTOnormal | causality | up-regulated | {
"name": "expression",
"pos": [
132,
141
],
"type": "Gene_expression"
} | {
"name": "suppression",
"pos": [
113,
123
],
"type": "Negative_regulation"
} |
19879420.s2 | For example, some studies showed that CLU expression is increased in advanced stages of prostate cancer and that suppression of CLU expression sensitizes prostate cancer cells to chemotherapeutic drugs killing. | prostate | {
"name": "CLU",
"pos": [
38,
40
]
} | {
"name": "prostate cancer",
"pos": [
88,
102
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
42,
51
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
56,
64
],
"type": "Positive_regulation"
} |
19879420.s3 | In contrast with the hypothesis that CLU is a positive modulator of prostate cancer, we and others have observed that CLU is downregulated during human prostate cancer progression. | prostate | {
"name": "CLU",
"pos": [
118,
120
]
} | {
"name": "prostate cancer",
"pos": [
68,
82
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "downregulated",
"pos": [
125,
137
],
"type": "Negative_regulation"
} |
19879420.s4 | Accordingly, a meta-analysis of available microarray data shows that CLU mRNA is significantly downregulated in prostate cancer tissue compared to normal prostate in 14 out of 15 independent studies. | prostate | {
"name": "CLU mRNA",
"pos": [
69,
76
]
} | {
"name": "prostate cancer",
"pos": [
112,
126
]
} | decreased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "downregulated",
"pos": [
95,
107
],
"type": "Negative_regulation"
} |
19879420.s6 | Consistently, CLU expression was found to be significantly reduced in untreated and hormone-refractory human prostate carcinomas. | prostate | {
"name": "CLU",
"pos": [
14,
16
]
} | {
"name": "prostate carcinomas",
"pos": [
109,
127
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
18,
27
],
"type": "Gene_expression"
} | {
"name": "reduced",
"pos": [
59,
65
],
"type": "Negative_regulation"
} |
21479359.s10 | In PC-3 cells, adhesion molecule expression, analyzed by immunoblotting, was unaffected by LA, while a down-regulation of c-met (up to 28%) was observed after 24 h of treatment but which did not hold up over time (48-144 h). | prostate | {
"name": "c-met",
"pos": [
122,
126
]
} | {
"name": "PC-3",
"pos": [
3,
6
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "down-regulation",
"pos": [
103,
117
],
"type": "Negative_regulation"
} |
||
21479359.s11 | Our findings demonstrate the efficacy of LA in upregulating E-cadherin, β- and γ-catenin in LNCaP cells. | prostate | {
"name": "E-cadherin",
"pos": [
60,
69
]
} | {
"name": "LNCaP",
"pos": [
92,
96
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "upregulating",
"pos": [
47,
58
],
"type": "Positive_regulation"
} |
||
21479359.s11 | Our findings demonstrate the efficacy of LA in upregulating E-cadherin, β- and γ-catenin in LNCaP cells. | prostate | {
"name": "γ-catenin",
"pos": [
79,
87
]
} | {
"name": "LNCaP",
"pos": [
92,
96
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "upregulating",
"pos": [
47,
58
],
"type": "Positive_regulation"
} |
||
12603425.s3 | In BPH samples there was a significant correlation between CD38 loss (mean 21% of acini) and HLA-DR up-regulation (mean 20%; P < 0.001). | prostate | {
"name": "HLA-DR",
"pos": [
93,
98
]
} | {
"name": "BPH",
"pos": [
3,
5
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "up-regulation",
"pos": [
100,
112
],
"type": "Positive_regulation"
} |
12603425.s4 | Moreover, 76% of all CD38-negative acini in BPH had HLA-DR up-regulation in the same prostate epithelial cells, predominantly in atrophic and cystic glands, and in cells with retained secretions (74%). | prostate | {
"name": "HLA-DR",
"pos": [
52,
57
]
} | {
"name": "BPH",
"pos": [
44,
46
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "up-regulation",
"pos": [
59,
71
],
"type": "Positive_regulation"
} |
12603425.s8 | The absence of CD38 and presence of HLA-DR expression in prostatic epithelium is consistent in BPH and tissue surrounding tumour, and strongly related to gland atrophy. | prostate | {
"name": "CD38",
"pos": [
15,
18
]
} | {
"name": "BPH",
"pos": [
95,
97
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "absence",
"pos": [
4,
10
],
"type": "Negative_regulation"
} |
||
14665875.s1 | The prostate cancer detection rate in patients with elevated prostate specific antigen (PSA) increases with extended needle biopsy protocols. | prostate | {
"name": "prostate specific antigen",
"pos": [
61,
85
]
} | {
"name": "prostate cancer",
"pos": [
4,
18
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "elevated",
"pos": [
52,
59
],
"type": "Positive_regulation"
} |
||
14665875.s1 | The prostate cancer detection rate in patients with elevated prostate specific antigen (PSA) increases with extended needle biopsy protocols. | prostate | {
"name": "PSA",
"pos": [
88,
90
]
} | {
"name": "prostate cancer",
"pos": [
4,
18
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "elevated",
"pos": [
52,
59
],
"type": "Positive_regulation"
} |
||
15193259.s1 | R-etodolac, a nonsteroidal anti-inflammatory drug, inhibits the progression of CWRSA6 androgen-independent and LuCaP-35 androgen-dependent prostate cancer xenograft growth through downregulation of cyclin D1 expression via the PPARgamma pathway. | prostate | {
"name": "cyclin D1",
"pos": [
198,
206
]
} | {
"name": "prostate cancer",
"pos": [
139,
153
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "expression",
"pos": [
208,
217
],
"type": "Gene_expression"
} | {
"name": "downregulation",
"pos": [
180,
193
],
"type": "Negative_regulation"
} |
17143532.s0 | Constitutive activation of MAPK/ERK inhibits prostate cancer cell proliferation through upregulation of BRCA2. | prostate | {
"name": "BRCA2",
"pos": [
104,
108
]
} | {
"name": "prostate cancer",
"pos": [
45,
59
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "upregulation",
"pos": [
88,
99
],
"type": "Positive_regulation"
} |
19483721.s0 | Overexpressing PKIB in prostate cancer promotes its aggressiveness by linking between PKA and Akt pathways. | prostate | {
"name": "PKIB",
"pos": [
15,
18
]
} | {
"name": "prostate cancer",
"pos": [
23,
37
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "Overexpressing",
"pos": [
0,
13
],
"type": "Gene_expression"
} | {
"name": "Overexpressing",
"pos": [
0,
13
],
"type": "Positive_regulation"
} |
15647840.s8 | DHT-induced E2F-1 protein and mRNA expressions was also inhibited by BMP-2, suggesting that BMP-2 inhibits DHT-induced growth of LNCaP cells through a decrease in E2F protein expression and suppression of E2F activity by hypophosphorylation of Rb. | prostate | {
"name": "E2F",
"pos": [
205,
207
]
} | {
"name": "LNCaP",
"pos": [
129,
133
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "suppression",
"pos": [
190,
200
],
"type": "Negative_regulation"
} |
15647840.s8 | DHT-induced E2F-1 protein and mRNA expressions was also inhibited by BMP-2, suggesting that BMP-2 inhibits DHT-induced growth of LNCaP cells through a decrease in E2F protein expression and suppression of E2F activity by hypophosphorylation of Rb. | prostate | {
"name": "E2F protein",
"pos": [
163,
173
]
} | {
"name": "LNCaP",
"pos": [
129,
133
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "expression",
"pos": [
175,
184
],
"type": "Gene_expression"
} | {
"name": "decrease",
"pos": [
151,
158
],
"type": "Negative_regulation"
} |
15647840.s8 | DHT-induced E2F-1 protein and mRNA expressions was also inhibited by BMP-2, suggesting that BMP-2 inhibits DHT-induced growth of LNCaP cells through a decrease in E2F protein expression and suppression of E2F activity by hypophosphorylation of Rb. | prostate | {
"name": "E2F-1 protein",
"pos": [
12,
24
]
} | {
"name": "LNCaP",
"pos": [
129,
133
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibited",
"pos": [
56,
64
],
"type": "Negative_regulation"
} |
21789713.s0 | Dual blockade of PKA and NF-κB inhibits H2 relaxin-mediated castrate-resistant growth of prostate cancer sublines and induces apoptosis. | prostate | {
"name": "PKA",
"pos": [
17,
19
]
} | {
"name": "prostate cancer",
"pos": [
89,
103
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "blockade",
"pos": [
5,
12
],
"type": "Negative_regulation"
} |
21789713.s0 | Dual blockade of PKA and NF-κB inhibits H2 relaxin-mediated castrate-resistant growth of prostate cancer sublines and induces apoptosis. | prostate | {
"name": "NF-κB",
"pos": [
25,
29
]
} | {
"name": "prostate cancer",
"pos": [
89,
103
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "blockade",
"pos": [
5,
12
],
"type": "Negative_regulation"
} |