Insight into the effects of microRNA-23a-3p on pancreatic cancer and its underlying molecular mechanism

Abstract

Previous studies have demonstrated that microRNA (miR)-23a-3p plays a role as an oncogene that is involved in several different types of carcinoma. However, few studies investigated the association between miR-23a-3p and pancreatic cancer (PC). The aim of the present study was to elucidate the biological functions of miR-23a-3p in PC and to investigate its underlying molecular mechanisms. The expression of miR-23a-3p in PC and adjacent normal tissues was investigated using microarrays. In order to validate the outcomes of the microarray results, reverse transcription-quantitative (RT-q)PCR was used to determine the expression levels of miR-23a-3p in PC tissues and cell lines. Furthermore, functional analyses were conducted following miR-23a-3p inhibition and overexpression, in order to assess the proliferation, invasion and migration of PC cells. Bioinformatics analysis indicated transforming growth factor-β receptor type II (TGFBR2) as a potential direct target of miR-23a-3p. Western blotting was performed in order to determine the protein expression of TGFBR2 in PC cell lines. The findings from the microarray demonstrated upregulation of miR-23a-3p in PC compared with normal tissues. RT-qPCR revealed significantly higher levels of miR-23a-3p expression in PC compared with normal control tissues or cells. Furthermore, miR-23a-3p was demonstrated to promote the proliferation, invasion and migration of PC cells, which was suppressed by the inhibition of miR-23a-3p. In addition, the miR-23a-3p expression level was negatively associated with TGFBR2 expression. Overall, the present study demonstrated the tumor-promoting effects of miR-23a-3p in PC cells. Furthermore, miR-23a-3p is a potential oncogenic regulator of PC, by targeting TGFBR2, and a biomarker or target for molecular therapy.