MiR-23a promotes cell proliferation and invasion in papillary thyroid carcinoma by targeting PTEN

Accumulating evidence has suggested that microRNAs (miRNAs) are involved in multiple processes in cancer development and progression by negatively regulating gene expression at posttranscriptional level. Recent studies have shown that miR-23a functions as an oncogene in many types cancer, but its role in papillary thyroid carcinoma (PTC) remains poorly understood. The aim of this study is to investigate the role and underling molecular mechanism of miR-23a in PTC. Here, we demonstrated that miR-23a is frequently upregulated in PTC specimens compared with adjacent noncancerous tissues. Function assay showed that restoration of miR-23a in PTC cells markedly promoted cell proliferation, migration and invasion, and inhibited PTC apoptosis. Bioinformatics analysis showed phosphatase and tensin homolog (PTEN) as a potential target of miR-23a. Data from luciferase reporter assays further confirmed that miR-23a directly binds to the 3’UTR of PTEN messenger RNA (mRNA). Furthermore, we found that overexpression of miR-23a suppressed PTEN expression at both transcriptional and translational levels in PTC cells. We also confirmed that PTEN expression on mRNA level was decreased in PTC tissue, and was inversely correlated miR-23a expression in PTC tissue. These findings suggested that miR-23a, acting as an oncogenic regulator by directly targeting PTEN in PTC, is a useful potential treatment target of papillary thyroid carcinoma.