4.3 Article

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

期刊

ONCOTARGET
卷 8, 期 12, 页码 19342-19353

出版社

IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.14258

关键词

prostate cancer; HnRNP-L; proliferation; apoptosis; molecular mechanism

资金

  1. Guangdong Provincial Science and Technology Program Planning Project [2013B021800147, 1311220700157, 2014A020212039, c1430611500534]
  2. ShenZhen Science and Technology Program Planning Project of ShenZhen City [20140323125307450, 201404153000668]

向作者/读者索取更多资源

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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