Phosphatase and tensin homolog (PTEN) loss is a major contributing factor of prostate cancer (PC). miRNA-1297 was reported to serve role in various cancer types; however, the potential roles of miRNA-1297 in PC had not been investigated. In the present study, tumor and adjacent tissues were collected from patients with PC. The gene expression level of miRNA-1297 was measured via polymerase chain reaction. Results indicated that the miRNA-1297 was overexpressed in tumor tissues from PC patients and in PC cell lines. miRNA-1297 also contributed toward the progression of PC. PTEN was confirmed as the direct target of miRNA-1297 and bound with miRNA-1297 via four binding sites. The miRNA-1297 level was negatively associated with the PTEN level. Silencing miRNA-1297 or overexpression of PTEN significantly inhibited the cell migration and invasion. In addition, the AKT/ERK pathway was also inhibited following silencing of miRNA-1297 or overexpression of PTEN. Taken together, the results indicated that silencing miRNA-1297 exerted inhibitory effects on the invasion and migration of PC cells via modulating PTEN and blocking of the AKT/ERK pathway. The results of the present study provided a novel strategy for treatment of prostate cancer cells.
Keywords: AKT/ERK pathway; PTEN; miRNA-1297; prostate cancer.
Copyright: © Wang et al.