|
Prostate carcinoma
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
After knocking down ARA55 expression in PZ-old cells, the PCa growth- promoting effect from the PZ-old cells was diminished, which may be explained by the decreased the progressive cytokines secretion (FGF-2, KGF, IGF-1) from PZ-old stromal cells.
|
27178620 |
2016 |
|
Prostate carcinoma
|
0.090 |
Biomarker
|
disease |
BEFREE |
Hic-5 acts as a coregulator with distinct effects on VDR transactivation, in prostate cancer and stromal cells, and may exert diverse effects on adjuvant therapy designed to exploit VDR activity in prostate cancer.
|
24825850 |
2014 |
|
Prostate carcinoma
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
Enforced expression of Hic-5 reverses the ability of Smad7 to suppress TGF-beta-induced phosphorylation of Smads 2 and 3 and activation of the plasminogen activator inhibitor-1 promoter (in NRP-154 and PC3 prostate carcinoma and WPMY-1 prostate myofibroblast cell lines).
|
18762808 |
2008 |
|
Prostate carcinoma
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
Because interaction of AR with the coactivator, Hic-5/ARA55, results in enhanced androgen-induced transcription, we analyzed Hic-5/ARA55 expression in prostate tissue sections from normal human donors and prostate cancer patients.
|
16849583 |
2006 |
|
Prostate carcinoma
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
ARA55 expression level in HRPC specimens was significantly lower than that in previously untreated prostate cancer (P = 0.02) or BPH (P = 0.005) samples using quantitative PCR.
|
12858356 |
2003 |
|
Prostate carcinoma
|
0.090 |
Biomarker
|
disease |
BEFREE |
Taken together, these findings not only demonstrate the important roles of the ARA55 coregulator in the AR-mediated growth of prostate cancer, they also may provide a critical target for developing therapeutic agents for the antiandrogen therapy that almost always fails in the treatment of hormone-refractory prostate cancer.
|
12700349 |
2003 |
|
Prostate carcinoma
|
0.090 |
Biomarker
|
disease |
BEFREE |
Characterization of the functional relationship between the AR and these coregulators indicated that ARA70 and ARA55 could enhance the androgenic effects of 17beta-estradiol (E2) and hydroxyflutamide (HF), an antiandrogen commonly used in the treatment of prostate cancer.
|
11501969 |
2002 |
|
Prostate carcinoma
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
Only ARA70 and ARA55 were able to significantly increase the androgenic activity of hydroxyflutamide, the active metabolite of a widely-used antiandrogen for the treatment of prostate cancer.
|
11155740 |
2000 |
|
Prostate carcinoma
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
Transient transfection assay in prostate cancer DU145 cells further demonstrates that ARA55 can enhance AR transcriptional activity in the presence of 1 nM dihydrotestosterone or its antagonists such as 100 nM 17beta-estradiol or 1 microM hydroxyflutamide.
|
10075738 |
1999 |
|
Malignant neoplasm of prostate
|
0.080 |
AlteredExpression
|
disease |
BEFREE |
After knocking down ARA55 expression in PZ-old cells, the PCa growth- promoting effect from the PZ-old cells was diminished, which may be explained by the decreased the progressive cytokines secretion (FGF-2, KGF, IGF-1) from PZ-old stromal cells.
|
27178620 |
2016 |
|
Malignant neoplasm of prostate
|
0.080 |
Biomarker
|
disease |
BEFREE |
Hic-5 acts as a coregulator with distinct effects on VDR transactivation, in prostate cancer and stromal cells, and may exert diverse effects on adjuvant therapy designed to exploit VDR activity in prostate cancer.
|
24825850 |
2014 |
|
Malignant neoplasm of prostate
|
0.080 |
AlteredExpression
|
disease |
BEFREE |
Because interaction of AR with the coactivator, Hic-5/ARA55, results in enhanced androgen-induced transcription, we analyzed Hic-5/ARA55 expression in prostate tissue sections from normal human donors and prostate cancer patients.
|
16849583 |
2006 |
|
Malignant neoplasm of prostate
|
0.080 |
AlteredExpression
|
disease |
BEFREE |
ARA55 expression level in HRPC specimens was significantly lower than that in previously untreated prostate cancer (P = 0.02) or BPH (P = 0.005) samples using quantitative PCR.
|
12858356 |
2003 |
|
Malignant neoplasm of prostate
|
0.080 |
Biomarker
|
disease |
BEFREE |
Taken together, these findings not only demonstrate the important roles of the ARA55 coregulator in the AR-mediated growth of prostate cancer, they also may provide a critical target for developing therapeutic agents for the antiandrogen therapy that almost always fails in the treatment of hormone-refractory prostate cancer.
|
12700349 |
2003 |
|
Malignant neoplasm of prostate
|
0.080 |
Biomarker
|
disease |
BEFREE |
Characterization of the functional relationship between the AR and these coregulators indicated that ARA70 and ARA55 could enhance the androgenic effects of 17beta-estradiol (E2) and hydroxyflutamide (HF), an antiandrogen commonly used in the treatment of prostate cancer.
|
11501969 |
2002 |
|
Malignant neoplasm of prostate
|
0.080 |
AlteredExpression
|
disease |
BEFREE |
Only ARA70 and ARA55 were able to significantly increase the androgenic activity of hydroxyflutamide, the active metabolite of a widely-used antiandrogen for the treatment of prostate cancer.
|
11155740 |
2000 |
|
Malignant neoplasm of prostate
|
0.080 |
AlteredExpression
|
disease |
BEFREE |
Transient transfection assay in prostate cancer DU145 cells further demonstrates that ARA55 can enhance AR transcriptional activity in the presence of 1 nM dihydrotestosterone or its antagonists such as 100 nM 17beta-estradiol or 1 microM hydroxyflutamide.
|
10075738 |
1999 |
|
Tumor Cell Invasion
|
0.060 |
Biomarker
|
phenotype |
BEFREE |
Compared to the control group, Hic-5 inhibition significantly reduced proliferation, increased apoptosis, and reduced invasion and migration of PCCs.
|
31683179 |
2020 |
|
Tumor Cell Invasion
|
0.060 |
Biomarker
|
phenotype |
BEFREE |
Collectively, our data highlight a novel role for Hic-5 in orchestrating the organization of invadopodia into higher-order rosettes, which may promote the localized matrix degradation necessary for tumor cell invasion.
|
30893012 |
2019 |
|
Tumor Cell Invasion
|
0.060 |
Biomarker
|
phenotype |
BEFREE |
HIC-5 knockdown in CAFs inhibited the migration and invasion of ESCC cells in vitro.
|
31740661 |
2019 |
|
Tumor Cell Invasion
|
0.060 |
AlteredExpression
|
phenotype |
BEFREE |
Our findings showed that Hic-5 over-expression could significantly induce increases in cell viability, migration and invasion, and induce decrease in cell apoptosis after hypoxia damage.
|
29864957 |
2018 |
|
Tumor Cell Invasion
|
0.060 |
AlteredExpression
|
phenotype |
BEFREE |
Domain mapping studies reveal sites critical to the functions of both Hic-5 and paxillin in regulating phenotype, while ectopic expression of Hic-5 in cell lines with low endogenous levels of the protein is sufficient to induce a Rac1-dependent mesenchymal phenotype and, in turn, increase amoeboid-mesenchymal plasticity and invasion.
|
29771639 |
2018 |
|
Tumor Cell Invasion
|
0.060 |
Biomarker
|
phenotype |
BEFREE |
Hic-5, a focal adhesion scaffold protein, has previously been implicated in tumor cell invasion, proliferation and metastasis.
|
27893716 |
2017 |
|
Neoplasms
|
0.050 |
AlteredExpression
|
group |
BEFREE |
HIC-5 was highly expressed in CAFs from the tumor stroma of human ESCC patients.
|
31740661 |
2019 |
|
Neoplasms
|
0.050 |
AlteredExpression
|
group |
BEFREE |
Interestingly, elevated Hic-5 expression correlates with reduced distant metastasis-free survival in patients with basal-like, HER2+ and grade 3 tumors.
|
29348458 |
2018 |