Research Papers:

HnRNP-L promotes prostate cancer progression by enhancing cell cycling and inhibiting apoptosis

Xumin Zhou, Qi Li, Jincan He, Liren Zhong, Fangpeng Shu, Rongwei Xing, Daojun Lv, Bin Lei, Bo Wan, Yu Yang, Huayan Wu, Xiangming Mao _ and Yaguang Zou

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Oncotarget. 2017; 8:19342-19353. https://doi.org/10.18632/oncotarget.14258

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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

Correspondence to:

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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