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Sci Rep. 2017 Mar 2;7:43683. doi: 10.1038/srep43683.

RNF7 knockdown inhibits prostate cancer tumorigenesis by inactivation of ERK1/2 pathway.

Xiao Y1,2,3, Jiang Y1,4, Song H1, Liang T1, Li Y1, Yan D1, Fu Q1, Li Z1.

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Shanghai Sixth People's Hospital East, Shanghai University of Medicine &Health Sciences, Shanghai 201306, China.
Joint Research Center for Translational Medicine, East China Normal University and Shanghai Fengxian District Central Hospital, Southern Medical University, Nanfeng Road 6600, Shanghai 201499, China.
Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, China.
Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China.


Development of castration resistance is a key contributor to mortality in patients with prostate cancer. High expression of RING finger protein 7 (RNF7) in cancer cells is known to play a key role in tumor progression. However, the role of RNF7 in prostate cancer progression is not well elucidated. In this study, we silenced RNF7 by shRNA interference in two castration resistant prostate cancer (CRPC) cell lines, DU145 and PC3. RNF7 knockdown attenuated proliferation and enhanced sensitivity of prostate cancer cells to cisplatin treatment. Invasive property of DU145 and PC3 cells was also attenuated by RNF7 silencing. The underlying mechanisms appear to be associated with accumulation of tumor suppressive proteins p21, p27 and NOXA, while inactivation of ERK1/2 by RNF7 knockdown. We demonstrated that RNF7 knockdown induced growth suppression of prostate cancer cells and inactivated ERK1/2 pathway, which suggested RNF7 might be a potential novel therapeutic target for CRPC.

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