MicroRNA-328 enhances cellular motility through posttranscriptional regulation of PTPRJ in human hepatocellular carcinoma.

Interaction between microRNA (miR-328) and PTPRJ (protein tyrosine phosphatase, receptor type, J) has been reported to be responsible for miR-328-dependent increase in epithelial cancer cell proliferation. However, the role of miR-328 and PTPRJ in hepatocellular carcinoma (HCC) remains unclear. The aim of this study was to investigate the clinical significance of miR-328 and/or PTPRJ expression in human HCC and determine their precise biological functions in this malignancy. Expression levels of miR-328 and PTPRJ messenger RNA (mRNA) in 100 pairs of HCC and adjacent noncancerous tissues were detected using quantitative real-time reverse transcription polymerase chain reaction. The associations between miR-328 and/or PTPRJ expression and various clinicopathological features of HCC patients were further statistically assessed. Then, the functions of miR-328 and PTPRJ in migration and invasion of two human HCC cell lines were determined by transwell assays. miR-328 and PTPRJ mRNA expression levels were markedly upregulated and down-regulated in HCC tissues, respectively, compared to adjacent noncancerous tissues. Notably, the upregulation of miR-328 in HCC tissues was significantly correlated with the downregulation of PTPRJ mRNA in HCC tissues (r=-0.362, P=0.01). In addition, miR-328-high and/or PTPRJ-low expression were found to be closely correlated with high Edmondson-Steiner grading (all P<0.05) and advanced tumor-node-metastasis stage (all P<0.05). Moreover, the restoration of miR-328 dramatically promoted HCC cell migration and invasion by repressing PTPRJ expression. Interestingly, the loss of PTPRJ expression could significantly attenuate the inhibitory effects of knockdown miR-328 on the migration and invasion of HCC cells. These findings demonstrated that the dysregulation of miR-328 and PTPRJ may be associated with tumor progression of HCC patients. Functionally, miR-328 may serve as a crucial oncogene and be implicated in the motility of HCC cells at least in part by the suppression of PTPRJ.