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Knockdown of GSG2 inhibits prostate cancer progression in vitro and in vivo.

ABSTRACT: Prostate cancer (PCa) is the second leading cause of cancer?related death among men worldwide. The present study aimed to investigate the role of germ cell?specific gene 2 protein (GSG2), also termed histone H3 phosphorylated by GSG2 at threonine?3, in the development and progression of PCa. GSG2 expression levels in PCa tissues and para?carcinoma tissues was detected by immunohistochemistry. The GSG2 knockdown cell model was constructed by lentivirus infection, and the knockdown efficiency was verified by qPCR and WB. In addition, the effects of shGSG2 on cell proliferation, colony formation and apoptosis were evaluated by Celigo cell counting assay, Giemsa staining and flow cytometry, respectively. Tumor development in nude mice was also detected. GSG2 expression was upregulated in PCa tissues and human PCa cell lines PC?3 and DU 145. High expression of GSG2 in tumor samples was associated with progressed tumors. GSG2 knockdown suppressed cell proliferation and colony formation, but promoted apoptosis, which was also verified in vivo. The results of the present study revealed that GSG2 upregulation was associated with PCa progression; GSG2 knockdown inhibited cell proliferation and colony formation and induced apoptosis, and may therefore serve as a potential therapeutic target for PCa therapy.

SUBMITTER: Yu F

PROVIDER: S-EPMC7252458 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

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Knockdown of GSG2 inhibits prostate cancer progression in vitro and in vivo.

Yu Feng F Lin Yuanyuan Y Xu Xinping X Liu Weipeng W Tang Dan D Zhou Xiaochen X Wang Gongxian G Zheng Yi Y Xie An A

International journal of oncology 20200413 1

Prostate cancer (PCa) is the second leading cause of cancer‑related death among men worldwide. The present study aimed to investigate the role of germ cell‑specific gene 2 protein (GSG2), also termed histone H3 phosphorylated by GSG2 at threonine‑3, in the development and progression of PCa. GSG2 expression levels in PCa tissues and para‑carcinoma tissues was detected by immunohistochemistry. The GSG2 knockdown cell model was constructed by lentivirus infection, and the knockdown efficiency was ...[more]

PMID: 32319597

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Project description:BackgroundCastration-resistant prostate cancer (CRPC) is currently the main challenge for prostate cancer (PCa) treatment, and there is an urgent need to find novel therapeutic targets and drugs. Prohibitin (PHB1) is a multifunctional chaperone/scaffold protein that is upregulated in various cancers and plays a pro-cancer role. FL3 is a synthetic flavagline drug that inhibits cancer cell proliferation by targeting PHB1. However, the biological functions of PHB1 in CRPC and the effect of FL3 on CRPC cells remain to be explored.MethodsSeveral public datasets were used to analyze the association between the expression level of PHB1 and PCa progression as well as outcome in PCa patients. The expression of PHB1 in human PCa specimens and PCa cell lines was examined by immunohistochemistry (IHC), qRT-PCR, and Western blot. The biological roles of PHB1 in castration resistance and underlying mechanisms were investigated by gain/loss-of-function analyses. Next, in vitro and in vivo experiments were conducted to investigate the anti-cancer effects of FL3 on CRPC cells as well as the underlying mechanisms.ResultsPHB1 expression was significantly upregulated in CRPC and was associated with poor prognosis. PHB1 promoted castration resistance of PCa cells under androgen deprivation condition. PHB1 is an androgen receptor (AR) suppressive gene, and androgen deprivation promoted the PHB1 expression and its nucleus-cytoplasmic translocation. FL3, alone or combined with the second-generation anti-androgen Enzalutamide (ENZ), suppressed CRPC cells especially ENZ-sensitive CRPC cells both in vitro and in vivo. Mechanically, we demonstrated that FL3 promoted trafficking of PHB1 from plasma membrane and mitochondria to nucleus, which in turn inhibited AR signaling as well as MAPK signaling, yet promoted apoptosis in CRPC cells.ConclusionOur data indicated that PHB1 is aberrantly upregulated in CRPC and is involved in castration resistance, as well as providing a novel rational approach for treating ENZ-sensitive CRPC.

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Knockdown of GSG2 inhibits prostate cancer progression in vitro and in vivo.

Publications

Knockdown of GSG2 inhibits prostate cancer progression in vitro and in vivo.

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