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Prostate cancer gene expression marker 1 ( PCGEM1 ) is a long non-coding RNA (lncRNA) overexpressed in prostate cancer (PCa) cells that promotes PCa initiation and progression, and protects against chemotherapy-induced apoptosis. The microRNA  miR-145  functions as a tumor suppressor in PCa. We speculate that reciprocal regulation of  PCGEM1  and  miR-145 promote proliferation of LNCaP prostate cancer cells. To test this hypothesis,  the interaction between  PCGEM1  and  miR-145  was examined using a luciferase reporter assay. Expression levels  w ere selectively altered in LNCaP cells and noncancerous RWPE-1 prostate cells by transfection of  miR-145  or small interfering RNA sequences against (siRNA)  PCGEM1 . Relative expression levels were detected by RT-PCR, tumor cell growth and early apoptosis by the MTT assay and flow cytometry, respectively, and tumor cell migration and invasion properties by transwell assays. The effect of siRNA  PCGEM1  and  miR-145  transfection on prostate cancer growth in vivo was examined in the (nu/nu) mouse model.  PCGEM1  and  miR-145  exhibited reciprocal regulation; downregulation of PCGEM1 expression in LNCaP cells increased expression of  miR-145 , while overexpression of  miR-145  decreased  PCGEM1  expression. Transfection of the  miR-145  expression vector and siRNA  PCGEM1  inhibited tumor cell proliferation, migration, and invasion, and induced early apoptosis both in vitro. In contrast, there was no effect on RWPE-1 cells. We demonstrate a reciprocal negative control relationship between  PCGEM1  and  miR-145  that regulates both LNCaP cell proliferation and nu/nu PCa tumor growth. The results also identify  PCGEM1  and associated regulators as possible targets for PCa therapy.

Reciprocal regulation of PCGEM1 and miR-145promote proliferation of LNCaP prostate cancer cells