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Abstract
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.
Highlights
Prostate cancer (Pca) is the second most frequently diagnosed cancer and the fifth leading cause of cancer death in males [1]
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 prostate cancer (Pca)
Among 160 Pca tissues, the expression of HnRNP-L was negatively associated with the clinic pathological parameter: The positive rate of HnRNP-L was significantly increased in low pathological tissues, compared to high pathological tissues (P
Summary
Prostate cancer (Pca) is the second most frequently diagnosed cancer and the fifth leading cause of cancer death in males [1]. There is an urgent need to understand the processes promoting tumorigenesis and progression in Pca as a means of improving treatment. It is an abundant nuclear protein that has been identified as a global splicing regulator [4]. It participates in splicing, transportation and degradation of precursor mRNAs [5,6,7,8,9]. Using two-dimensional electrophoresis and www.impactjournals.com/oncotarget mass spectrometry, Zhao et al showed that HNRNP-L is differentially expressed in Pca [16]. The specific roles of HnRNP-L in Pca remain unclear. We investigated the effects of HnRNP-L expression on tumorigenesis and progression in Pca
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