Is involved in 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 first Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi 710061, P.R. China Received Ubiquitin Inhibitors medchemexpress September two, 2016; Accepted Indibulin web January 24, 2017 DOI: 10.3892/or.2017.5448 Abstract. Escalating quantity of studies report that microRNAs play important roles in radiosensitization. miR-30a has been proved to carry out numerous functions in the development and therapy of cancer, and it’s downregulated in non-small cell lung cancer (NSCLC) tissues and cells. This study was conducted to understand if miR-30a plays a part in the radiosensitivity of NSCLC cells. Radiosensitivity was examed by colony survival assay and tumor volume altering in vitro and in vivo, respectively. Bioinformatic evaluation and luciferase reporter assays were made use of to distinguish the candidate target of miR-30a. qRT-PCR and western blotting were carried out to detect the relative expression of mRNAs and proteins. Cell cycle and cell apoptosis have been determined by flow cytometry. Our results illustrated miR-30a could boost the radiosensitivity of NSCLC, particularly in A549 cell line. In vivo experiment also showed the potential radiosensitizing possibility of miR-30a. Further exploration validated that miR-30a was directly targeting activating transcription aspect 1 (ATF1). In studying the ataxia-telangiectasia mutated (ATM) linked effects on cell radiosensitivity, we discovered that miR-30a could lower radiation induced G2/M cell cycle arrest and may perhaps also influence radiation induced apoptosis. Together, our results demonstrated that miR-30a could modulate the radiosensitivity of NSCLC by way of minimizing the function of ATF1 in phosphorylation of ATM and have prospective therapeutic value. Introduction miR-30a has been implicated to function as tumor suppressor in various types of cancer (1), which include breast cancer (2), colon cancer (three), osteosarcoma (4), hepatocellular carcinoma (five), non-small cell lung cancer (NSCLC) (six), glioma (7), ovarian carcinoma (8) and renal clear cell carcinoma (9). Quite a few research have suggested that miR-30a could inf luence tumor progression by means of modulating cancer cell proliferation (10), migration, invasion (4), epithelial-mesenchymal transition (EMT) (2), apoptosis (five), autophagy (11) and other ways (12). A study on NSCLC tissues making use of 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 towards the similar conclusion and revealed that its low expression was associated with cancer risk and indicated poor prognosis (15). In vitro experiment (16) also recommended miR-30a was downregulated in NSCLC A549 cells compared with BEAS-2B regular lung epithelial cells, overexpression of miR-30a could inhibit A549 lung cancer cell malignancy (6,16). On the other hand, the exact function and underlying mechanism whereby miR-30a regulates the improvement and progression of NSCLC remains elusive. MicroRNAs have already been discovered to modulate tumor radiosensitivity in modulating various pathways and molecules (17,18). The main ways that miRNAs modulate radiosensitivity had been DNA damage repair, apoptosis, cell cycle checkpoint and tumor microenvironment (19). miR-124, miR-200c, miR-302 and miR-142 were identified to affect the radiosensitivity of colorectal cancer (20), NSCLC (21), breast cancer (22) and mal.