Effect and Mechanism of LncRNA-PBC11 in Regulating EMT Progression of Prostate Cancer Cells

Abstract The invasion and metastasis of prostate cancer is the main reason for its poor prognosis. Up to now, ADT (androgen deprivation therapy, ADT), whether surgical or drug therapy, is the basic method for the treatment of prostate cancer. However, ADT therapy is generally not recommended for the clinical treatment of metastatic prostate cancer. EMT (epithelial-to-mesenchymal transition, EMT) of tumor cells is the internal driving factor of tumor invasion and metastasis. Therefore, in-depth study on the regulation mechanism of EMT in prostate cancer cells will help us develop the new prevention and treatment plan for prostate cancer. Here, we will demonstrate and elaborate an lncRNA-PBC11 closely related to EMT of prostate cancer cells. The research data show that the content of PBC11 in metastatic prostate tumors increases significantly compared to non-metastatic, and can competitively bind hsa-miR-137 with 3'UTR of Twist1 in the form of miRNA sponge, thereby weakening the antitumor activity of hsa-miR-137. Our functional experiments confirmed that PBC11 knockdown is an important means for the normal operation of EMT inhibitory pathway hsa-miR-137/Twist1 in prostate cancer cells, and PBC11 knockdown combined with hsa-miR-137 overexpression showed excellent resistance to EMT in prostate cancer cells induced by TGF-β1. In a word, our study shows that PBC11 up-regulates the expression of Twist1 protein by blocking hsa-miR-137/ Twist1 pathway and promotes the progress of EMT in prostate cancer cells, overexpression of PBC11 can effectively inhibit EMT in prostate cancer cells by restoring the negative regulation of Twist1 by hsa-miR-137.