Effect and Mechanism of lncRNA-PCMF1/hsa-miR-137/Twist1 Axis Involved inthe EMTRegulation of Prostate Cancer Cells.

Abstract

The metastasis is a majorreason for the poor prognosis of the patients with prostate cancer (PC). Currently, androgen deprivation therapy (ADT) is the basic method for the treatment of PC regardless of surgery or drug treatments. However, ADT therapy is generally not recommended for patients with advanced/metastatic PC. Herein, wereportforthefirsttime a long non-coding RNA (lncRNA)-PCMF1 which promotes the progression of Epithelial-Mesenchymal Transition (EMT) in PC cells. Our data demonstrated that PCMF1 in metastatic PC tissues increased significantly compared to non-metastatic specimens. Mechanismresearchshowedthat PCMF1 could competitively bind to hsa-miR-137 instead of the 3' -Untranslated Region (UTR) of Twist Family BHLH Transcription Factor 1 (Twist1) by acting as an endogenous miRNA sponge. Furthermore,we found that silence of PCMF1 effectively blocked the EMT in PC cells by indirectly suppressing Twist1 protein mediated by hsa-miR-137 at post-transcriptional level. In summary, our research shows that PCMF1 promotes the EMT of PC cells by causing the functional inactivation of hsa-miR-137 on Twist1 protein, which is an independent risk factor of PC. PCMF1 knockdown combined with hsa-miR-137 expression is a promising PC-targeted therapy. Furthermore, PCMF1 is also expected toactas a useful marker for predicting malignantchanges and assessing the prognosis of PC patients.