Objective To investigate the effect of miR-107 on the function of human non-small cell lung cancer cell line A549 and its possible target genes.Methods The experiment was divided into the liposome+miR-107 mimics overexpression group(OV-miR-107 group),liposome+miR-107 inhibiting mimics downregulation group(KD-miR-107 group)and liposome+ negative control mimics group(NC group).The cell transfections of siRNA were siRNA-1,siRNA-2 and siRNA-3 respectively.The cellular prolifer-ation capacity was detected by MTT assay.The cellular cycle was detected by flow cytometry.The dual luciferase reporter gene as-say was performed to detect the downstream target gene of miR-107.The real time quantitative reverse transcription PCR and Western blot were respectively employed to examine mRNA and protein expression levels of downstream target gene.Results miR-107 inhibited the proliferation of A549 cells in a time-and dose-dependent manner(P<0.05).miR-107 arrested more A549 cells at the G0G1phase,and the proportions of S phase and G2M phase were decreased(P<0.05).miR-107 combinded with the 246 bp-253 bp of CCNE1 3′-untranslated region,and decreased mRNA and protein expression of CCNE1(P<0.05);after down-regulating CC-NE1 in A549 cells,siRNA-2 inhibited cellular proliferation(P<0.05)and blocked the cells to stay at G0G1phase(P<0.05).Con-clusion miR-107 inhibits the proliferation of human non-small cell lung cancer cell line A549 and regulates the cellular cycle by tar-geting CCNE1.

Radiotherapy is a first-line treatment for a variety of malignant tumors by inducing DNA damage to kill tumor cells. However, tumor cells have different sensitivities to radiotherapy, ultimately leading to different therapeutic effects. Histone acetylation, regulated by histone acetyltransferase (HAT) and histone deacetylase (HDAC), is involved in the regulation of cell radiation sensitivity by influencing DNA damage repair. The main mechanisms are recruiting DNA repair related proteins and mediating chromatin dynamic changes. In this article, the role of histone acetylation modification in tumor radiotherapy was reviewed, aming to provide the basis for the radiotherapy sensitization strategy based on histone acetylation.