SHARPIN overexpression induces tumorigenesis in human prostate cancer LNCaP, DU145 and PC-3 cells via NF-κB/ERK/Akt signaling pathway

• Published in: Medical oncology (Northwood, London, England) Vol. 32; no. 2; p. 444
• Main Authors: Li, Jin, Lai, Yiming, Cao, Yi, Du, Tao, Zeng, Lexiang, Wang, Ganping, Chen, Xianju, Chen, Jieqing, Yu, Yongsheng, Zhang, Simin, Zhang, Yiming, Huang, Hai, Guo, Zhenghui
• Format: Journal Article
• Language: English
• Published: Boston Springer US 01.02.2015; Springer Nature B.V
• Subjects: Apoptosis; Blotting, Western; Carcinogenesis - metabolism; Carcinogenesis - pathology; Cell Line, Tumor; Cell Proliferation - physiology; Cell Survival - physiology; Flow Cytometry; Hematology; Humans; Internal Medicine; Male; MAP Kinase Signaling System - physiology; Medicine; Medicine & Public Health; NF-kappa B - metabolism; Oncology; Original Paper; Pathology; Prostate cancer; Prostatic Neoplasms - pathology; Proto-Oncogene Proteins c-akt - metabolism; Real-Time Polymerase Chain Reaction; Signal Transduction - physiology; Transfection; Tumorigenesis; Ubiquitins - metabolism; Up-Regulation; Tumorigenesis; SHARPIN; NF-κB/ERK/Akt pathway; Prostate cancer; Apoptosis
• ISSN: 1357-0560; 1559-131X
• DOI: 10.1007/s12032-014-0444-3

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.