MiRNA-215-5p alleviates the metastasis of prostate cancer by targeting PGK1.

Abstract

MicroRNAs (miRNAs) are endogenous, non-coding RNAs, which exert crucial functions in regulating biological progressions. Previous studies have demonstrated the anti-tumor effect of miRNA-215-5p. However, its specific role in influencing the progression of prostate cancer (PCa) remains unclear. This study aims to uncover the regulatory effect of miRNA-215-5p on the metastasis and prognosis of PCa. MiRNA-215-5p levels in collected PCa tissues (n=52) and paracancerous tissues (n=52) were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The relationship between miRNA-215-5p level and pathological indexes, as well as overall survival of PCa patients, was analyzed. Regulatory effects of miRNA-215-5p on proliferative and metastatic capacities of LNCaP and DU-145 cells were evaluated through cell counting kit-8 (CCK-8) and transwell assay, respectively. Bioinformatics prediction was performed to search for the target genes of miRNA-215-5p and PGK1 was selected. The biological role of PGK1 in the progression of PCa was finally clarified by a series of rescue experiments. MiRNA-215-5p was lowly expressed in PCa tissues and cell lines. Low level of miRNA-215-5p predicted poor prognosis in PCa patients. The silence of miRNA-215-5p enhanced viability, migratory, and invasive capacities of LNCaP cells, while the overexpression of miRNA-215-5p yielded the opposite trends in DU-145 cells. PGK1 was predicted to be the target of miRNA-215-5p. PGK1 was upregulated in PCa tissues and cell lines and its high level predicted poor prognosis of PCa. Moreover, PGK1 level was negatively correlated to that of miRNA-215-5p in PCa tissues. PGK1 was able to reverse the regulatory effects of miRNA-215-5p on metastatic potentials of PCa cells. Downregulated miRNA-215-5p in PCa is closely related to distant metastasis and poor prognosis of affected patients. MiRNA-215-5p alleviates the malignant progression of PCa by targeting and downregulating PGK1.