miR-532-3p promotes hepatocellular carcinoma progression by targeting PTPRT

Background: Aberrant expression of miR-532-3p was involved in progression and development of multiple cancers, whereas miR-532-3p has not been reported in hepatocellular carcinoma (HCC). The aim of this study was to elucidate the functions of miR-532-3p in progression of HCC. Methods: Real-time PCR in HCC tissues and cell lines and database analysis were conducted for detection of the expression of miR-532-3p in HCC. Then, the association of miR-532-3p with clinicopathological features and prognosis of HCC patients were statistically measured. Subsequently, we attempted to observe the effects of miR-532-3p on migration, invasion and proliferation of HCC cells by Wound healing assay, Transwell assays, MTT assay and EdU assay. Furthermore, bioinformatics tools, database analysis, luciferase reporter gene assay and rescue experiments were conducted to explore the target of miR-532-3p in HCC, and to explore whether the target mediated the effects of miR-532-3p on HCC cells. Results: Our findings and data from databases consistently indicated that the miR-532-3p expression level was higher in HCC. In addition, high miR-532-3p expression was found to be closely related to larger tumor size (P = 0.0027), presence of vascular invasion (P = 0.015), and advanced TNM stage (P = 0.015). In addition, experiments in vitro revealed that miR-532-3p promotes migration, invasion and proliferation of HCC cells. Furthermore, receptor protein tyrosine phosphatase T (PTPRT) was identified as the target and mediator of miR-532-3p in HCC cells. Conclusion: Our results demonstrate that miR-532-3p, which is frequently up-regulated in HCC, contributes to HCC cells mobility and proliferation through targeting PTPRT.