Is involved within the phosphorylation of ATMYUYAN GUO, WENZE SUN, TUOTUO GONG, YANLAN CHAI, JUAN WANG, BEINA HUI, YI LI, LIPING SONG and YING GAO Department of Radiation Oncology, The very first Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi 710061, P.R. China Received September 2, 2016; Accepted January 24, 2017 DOI: 10.3892/or.2017.5448 Abstract. Growing variety of research report that microRNAs play significant roles in radiosensitization. miR-30a has been proved to carry out many functions within the development and remedy of cancer, and it truly is downregulated in non-small cell lung cancer (NSCLC) tissues and cells. This study was carried out to understand if miR-30a plays a function inside the radiosensitivity of NSCLC cells. Radiosensitivity was examed by colony survival assay and tumor volume altering in vitro and in vivo, respectively. Bioinformatic analysis and luciferase reporter assays had been made use of to distinguish the candidate target of miR-30a. qRT-PCR and western blotting had been carried out to detect the relative expression of mRNAs and proteins. Cell cycle and cell apoptosis were determined by flow cytometry. Our benefits illustrated miR-30a could improve the radiosensitivity of NSCLC, particularly in A549 cell line. In vivo experiment also showed the prospective radiosensitizing possibility of miR-30a. Further exploration validated that miR-30a was straight targeting activating transcription element 1 (ATF1). In studying the ataxia-telangiectasia mutated (ATM) connected effects on cell radiosensitivity, we found that miR-30a could lessen radiation induced G2/M cell cycle arrest and may well also have an effect on radiation induced apoptosis. Together, our benefits demonstrated that miR-30a could modulate the radiosensitivity of NSCLC by way of decreasing the function of ATF1 in phosphorylation of ATM and have potential therapeutic value. Introduction miR-30a has been implicated to function as tumor suppressor in numerous types of cancer (1), which include breast cancer (2), colon cancer (3), osteosarcoma (4), hepatocellular carcinoma (five), non-small cell lung cancer (NSCLC) (six), glioma (7), ovarian carcinoma (8) and renal clear cell carcinoma (9). Many research have suggested that miR-30a could inf luence tumor progression via modulating cancer cell proliferation (ten), migration, invasion (4), epithelial-mesenchymal transition (EMT) (two), apoptosis (5), autophagy (11) and other ways (12). A study on NSCLC tissues using miRNA microarray demonstrated that miR-30a was downregulated in each adenocarcinomas (14/20) and squamous cell carcinomas (20/20) (P=0.448) (13). Other research (14) arrived for the identical conclusion and revealed that its low expression was connected with cancer threat and indicated poor prognosis (15). In vitro experiment (16) also suggested miR-30a was downregulated in NSCLC A549 cells compared with BEAS-2B normal lung epithelial cells, overexpression of miR-30a could inhibit A549 lung cancer cell malignancy (6,16). Having said that, the exact part and underlying mechanism whereby miR-30a regulates the improvement and progression of NSCLC remains elusive. MicroRNAs have been located to modulate tumor radiosensitivity in modulating several different pathways and molecules (17,18). The main strategies that Clopamide miRNAs modulate radiosensitivity were DNA damage repair, apoptosis, cell cycle checkpoint and tumor microenvironment (19). miR-124, miR-200c, miR-302 and miR-142 were located to affect the radiosensitivity of colorectal cancer (20), NSCLC (21), breast cancer (22) and mal.