Long non‑coding RNA HCP5 promotes prostate cancer cell proliferation by acting as the sponge of miR‑4656 to modulate CEMIP expression.

Abstract

Aberrant expression of long noncoding RNAs (lncRNAs) has been demonstrated in human cancers and regulates the malignant behavior of cancer cells. Previous studies demonstrated the critical involvement of lncRNA histocompatibility leukocyte antigen (HLA) complex P5 (HCP5) in the development of cancers, however, the function of HCP5 in prostate cancer has not been reported. In the present study, we found the overexpressed expression of HCP5 in prostate cancer tissues and cell lines via RT‑qPCR analysis. High expression of HCP5 was positively correlated with the metastasis of prostate cancer. Downregulation of HCP5 inhibited the proliferation, colony formation and induced apoptosis of prostate cancer cells. Functional experiments demonstrated that HCP5 acted as a competing endogenous RNA (ceRNA) to sponge miR‑4656. Ectopic expression of HCP5 decreased the expression of miR‑4656 in prostate cancer cells. MiR‑4656 was found to be decreased in prostate cancer tissues and was negatively correlated with the expression of HCP5. Further luciferase reporter assay revealed that miR‑4656 was able to bind the 3'‑untranslated region (3'‑UTR) of the cell migration inducing hyaluronidase 1 (CEMIP) and suppressed the expression of CEMIP. Consistent with the negative regulation of miR‑4656 by HCP5, western blot analysis uncovered that overexpression of HCP5 upregulated the abundance of CEMIP in prostate cancer cells. The CCK‑8 assay showed that depletion of CEMIP significantly inhibited the HCP5‑promoted proliferation of prostate cancer cells. Collectively, our data provide a novel mechanism by which HCP5 regulates the progression of prostate cancer.