Is involved inside the phosphorylation of ATMYUYAN GUO, WENZE SUN, TUOTUO GONG, YANLAN CHAI, JUAN WANG, BEINA HUI, YI LI, LIPING SONG and YING GAO Division of Radiation Oncology, The very first Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi 710061, P.R. China Received September two, 2016; Accepted January 24, 2017 DOI: ten.3892/or.2017.5448 Abstract. Increasing number of studies report that microRNAs play important roles in radiosensitization. miR-30a has been proved to carry out lots of functions inside the development and treatment of cancer, and it is downregulated in non-small cell lung cancer (NSCLC) tissues and cells. This study was performed to understand if miR-30a plays a role within the radiosensitivity of NSCLC cells. Radiosensitivity was examed by colony survival assay and tumor volume changing in vitro and in vivo, respectively. Bioinformatic evaluation and luciferase reporter assays were applied to distinguish the candidate target of miR-30a. qRT-PCR and western blotting have been carried out to detect the relative expression of mRNAs and proteins. Cell cycle and cell apoptosis were determined by flow cytometry. Our outcomes illustrated miR-30a could enhance the radiosensitivity of NSCLC, particularly in A549 cell line. In vivo experiment also showed the possible radiosensitizing possibility of miR-30a. Further exploration validated that miR-30a was straight targeting activating transcription factor 1 (ATF1). In studying the ataxia-telangiectasia mutated (ATM) related effects on cell radiosensitivity, we found that miR-30a could decrease radiation induced G2/M cell cycle arrest and may also SI-2 Technical Information impact radiation induced apoptosis. Together, our final results demonstrated that miR-30a might modulate the radiosensitivity of NSCLC via lowering the function of ATF1 in phosphorylation of ATM and have possible therapeutic worth. Introduction miR-30a has been implicated to function as tumor suppressor in various types of cancer (1), including breast cancer (two), colon cancer (three), osteosarcoma (4), hepatocellular carcinoma (5), non-small cell lung cancer (NSCLC) (six), glioma (7), ovarian carcinoma (eight) and renal clear cell carcinoma (9). Many studies have recommended that miR-30a could inf luence tumor progression by way of modulating cancer cell proliferation (ten), migration, invasion (4), epithelial-mesenchymal transition (EMT) (2), apoptosis (5), autophagy (11) and other methods (12). A study on NSCLC tissues using miRNA microarray demonstrated that miR-30a was downregulated in both adenocarcinomas (14/20) and squamous cell carcinomas (20/20) (P=0.448) (13). Other studies (14) arrived towards the same conclusion and revealed that its low expression was associated with cancer danger and indicated poor prognosis (15). In vitro experiment (16) also suggested 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). Even so, the exact part and underlying mechanism whereby miR-30a regulates the improvement and progression of NSCLC remains elusive. MicroRNAs happen to be found to modulate tumor radiosensitivity in modulating various pathways and molecules (17,18). The main ways that miRNAs modulate radiosensitivity had been DNA harm repair, apoptosis, cell cycle checkpoint and tumor microenvironment (19). miR-124, Ctgf Inhibitors MedChemExpress miR-200c, miR-302 and miR-142 were discovered to affect the radiosensitivity of colorectal cancer (20), NSCLC (21), breast cancer (22) and mal.