Abstract
SHARPIN emerges higher expression in prostate cancerous tissues than in benign prostate hyperplasia by means of immunohistochemistry in our previous study. In this work, we performed the gain of function assay and find that overexpression of SHARPIN in LNCaP, DU145 and PC-3 cells promoted cell proliferation, invasiveness and reduced apoptosis. Furthermore, SHARPIN overexpression displayed elevated Bcl-2 and Survivin expression and reduced levels of Bax, cleaved caspase-3. Meanwhile, entropic expression of SHARPIN increased the levels of phosphorylated p65, IkBα, ERK and Akt, were selectively increased in these cells. Collectively, our study unraveled the ability of SHARPIN overexpression to induce tumorigenesis of prostate cancer cells through the NF-kB/ERK/Akt pathway and transformation of apoptosis-associated proteins.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
