scholarly journals The X-linked tumor suppressor TSPX downregulates cancer-drivers/oncogenes in prostate cancer in a C-terminal acidic domain dependent manner

Oncotarget ◽  
2019 ◽  
Vol 10 (15) ◽  
pp. 1491-1506 ◽  
Author(s):  
Tatsuo Kido ◽  
Yunmin Li ◽  
Yuichiro Tanaka ◽  
Rajvir Dahiya ◽  
Yun-Fai Chris Lau
Keyword(s):  
Prostate Cancer ◽  
Tumor Suppressor ◽  
Dependent Manner ◽  
Acidic Domain ◽  
Cancer Drivers

scholarly journals LRIG1 is a pleiotropic androgen receptor-regulated feedback tumor suppressor in prostate cancer

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Qiuhui Li ◽  
Bigang Liu ◽  
Hsueh-Ping Chao ◽  
Yibing Ji ◽  
Yue Lu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Suppressor ◽  
Tumor Development ◽  
Dependent Manner ◽  
Oncogenic Signaling ◽  
Transgenic Expression ◽  
Functional Studies ◽  
Castration Resistant ◽  
A Cell ◽  
Xenograft Models

AbstractLRIG1 has been reported to be a tumor suppressor in gastrointestinal tract and epidermis. However, little is known about the expression, regulation and biological functions of LRIG1 in prostate cancer (PCa). We find that LRIG1 is overexpressed in PCa, but its expression correlates with better patient survival. Functional studies reveal strong tumor-suppressive functions of LRIG1 in both AR+ and AR− xenograft models, and transgenic expression of LRIG1 inhibits tumor development in Hi-Myc and TRAMP models. LRIG1 also inhibits castration-resistant PCa and exhibits therapeutic efficacy in pre-established tumors. We further show that 1) AR directly transactivates LRIG1 through binding to several AR-binding sites in LRIG1 locus, and 2) LRIG1 dampens ERBB expression in a cell type-dependent manner and inhibits ERBB2-driven tumor growth. Collectively, our study indicates that LRIG1 represents a pleiotropic AR-regulated feedback tumor suppressor that functions to restrict oncogenic signaling from AR, Myc, ERBBs, and, likely, other oncogenic drivers.

scholarly journals Tumor Suppressor BRCA1 Is Expressed in Prostate Cancer and Controls Insulin-like Growth Factor I Receptor (IGF-IR) Gene Transcription in an Androgen Receptor–Dependent Manner

2009 ◽  
Vol 15 (5) ◽  
pp. 1558-1565 ◽  
Author(s):  
Hagit Schayek ◽  
Kathy Haugk ◽  
Shihua Sun ◽  
Lawrence D. True ◽  
Stephen R. Plymate ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Growth Factor ◽  
Tumor Suppressor ◽  
Gene Transcription ◽  
Dependent Manner ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I

Paeonol Inhibits Prostate Cancer Cell Invasion and Epithelial-Mesenchymal Transformation by Inactivation of STAT3 Pathway

2020 ◽  
Vol 19 (1) ◽  
pp. 15-20
Author(s):  
Junyi Xiang ◽  
Feng Huang ◽  
Renhua Huang ◽  
Jingzhan Su ◽  
Yulong Liu
Keyword(s):  
Prostate Cancer ◽  
Treatment Options ◽  
Surrogate Marker ◽  
Cytotoxic Agents ◽  
Potential Candidate ◽  
Dependent Manner ◽  
Ablation Therapy ◽  
Androgen Ablation ◽  
Mesenchymal Transformation ◽  
Dose Dependent

Prostate cancer is one of the leading causes of death in men all over the world. Treatment options such as androgen ablation therapy and cytotoxic agents have many undesirable side effects, narrow therapeutic windows, or other limitations. In this research, we have explored the effects of paeonol on prostate cancer and its mechanism of action. Our results have shown that paeonol reduced the viability of prostate cancer cells in a dose-dependent manner. The wound-healing assay, a surrogate marker of tumor metastasis, showed that the relative wound width of 10 µM group was less than that of 50 µM paeonol-treated cells. Besides, the results of the transwell assay also showed that the number of migrated cells was significantly lower after treatment with 50 µM paeonol compared to the 10 µM group. The Western blot results showed that paeonol treatment induced a decrease in the mesenchymal markers (vimentin and N-cadherin), while the epithelial marker (E-cadherin) increased in a dose-dependent manner suggesting that paeonol effectively inhibits the epithelial-mesenchymal transformation in PC3 cells. Furthermore, the expression of STAT3 and p-STAT3 was also decreased after paeonol treatment, which indicated that the STAT3 signaling pathway was inhibited by paeonol. To conclude, the results summarized in this paper suggest that paeonol could be a potential candidate in the treatment of prostate cancer.

The p202 Gene as a Tumor Suppressor in Prostate Cancer Cells

2003 ◽  
Author(s):  
Mien-Chie Hung
Keyword(s):  
Prostate Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Prostate Cancer Cells
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