HnRNP-L promotes prostate cancer progression by enhancing cell cycling and inhibiting apoptosis
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Xumin Zhou1,*, Qi Li4,*, Jincan He5,*, Liren Zhong1, Fangpeng Shu1, Rongwei Xing6, Daojun Lv1, Bin Lei1, Bo Wan1, Yu Yang2, Huayan Wu1, Xiangming Mao1,2, Yaguang Zou3
1Department of Urology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, P. R.China
2Department of Urology, Peking University Shenzhen Hospital, Shenzhen PKU-HKUST Medical Center, Shenzhen, 518036, P. R.China
3Department of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, P. R.China
4Department of Urology, Maternal and Health Care Hospital, Longgang District, Shenzhen 518036, P. R.China
5Department of Urology, Fourth Affiliated Hospital, Guangxi Medical University, Liuzhou 545005, P. R.China
6Department of Urology, Affiliated Weihai Second Municipal Hospital of Qingdao University, Weihai 264200, P. R.China
*These authors have contributed equally to this work
Xiangming Mao, email: [email protected]
Yaguang Zou, email: [email protected]
Keywords: prostate cancer, HnRNP-L, proliferation, apoptosis, molecular mechanism
Received: August 19, 2016 Accepted: December 01, 2016 Published: December 27, 2016
Expression of the RNA-binding protein HnRNP-L was previously shown to associate with tumorigenesis in liver and lung cancer. In this study, we examined the role of HnRNP-L in prostate cancer (Pca). We found that HnRNP-L is overexpressed in prostate tissue samples from 160 PC patients compared with tissue samples from 32 donors with cancers other than Pca. Moreover, HnRNP-L positively correlated with aggressive tumor characteristics. HnRNP-L knockdown inhibited cell proliferation and promoted cell apoptosis of Pca cell lines in vitro, and suppressed tumor growth when the cells were subcutaneously implanted in an athymic mouse model. Conversely, overexpression of HnRNP-L promoted cell proliferation and tumor growth while prohibiting cell apoptosis. HnRNP-L promoted cell proliferation and tumor growth in Pca in part by interacting with endogenous p53 mRNA, which was closely associated with cyclin p21. In addition, HnRNP-L affected cell apoptosis by directly binding the classical apoptosis protein BCL-2. These observations suggest HnRNP-L is an important regulatory factor that exerts pro-proliferation and anti-apoptosis effects in Pca through actions affecting the cell cycle and intrinsic apoptotic signaling. Thus HnRNP-L could potentially serve as a valuable molecular biomarker or therapeutic target in the treatment of Pca.
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