miR-106b enhances cell radioresistance by targeting PTEN in colorectal carcinoma / 中华放射肿瘤学杂志

ABSTRACT

Objective:To investigate the role of miR-106b in the cell radioresistance in colorectal carcinoma (CRC), and unravel the underlying mechanism.Methods:The CRC cell lines stably overexpressing and interfering miR-106b were established. The effect of miR-106b upon the CRC cell radiosensitivity was evaluated by cell radiation, immunofluorescence and colony formation assay. The expression levels of Caspase-3 and γ-H 2AX were detected by Western blot. The target genes of miR-106b were identified by bioinformatics prediction, which were further validated by dual luciferase assay, fluorescence quantitative PCR and Western blot. The CRC cell lines stably overexpressing miR-106b were transfected with pCDNA3.0-PTEN. The changes of CRC cell radiosensitivity were investigated. Whether miR-106b could increase the radioresistance of CRC cells by targeting PTEN was clarified. Results:Compared with the control group (miR-ctr group), the cell surviving fraction was significantly elevated ( P<0.05), the radioresistance ( P<0.05) was considerably enhanced and the expression levels of Caspase-3 and γ-H 2AX were significantly down-regulated (both P<0.05) in the miR-106b overexpression group. PTEN up-regulation in CRC cell lines stably overexpressing miR-106b could reverse the radioresistance induced by miR-106b. Conclusion:miR-106b can induce CRC cell radioresistance by inhibiting PTEN, prompting that miR-106b-PTEN might provide theoretical evidence for relevant targets which can enhance the clinical efficacy of radiotherapy.