Preliminary Study On The Effects And Mechanisms Of MiR-26b On Radiation-induced Lung Injury

Radiation-induced lung injury is the serious complicated disease in mammography after radiotherapy.Radiation pneumonia is the early symptoms,and pμlmonary fibrosis is the anaphasis symptoms.Radiation-induced lung injury reduce the patients,quality of life and shorten the patient disease-free survival.MicroRNAs,a group of endogenous small non-coding RNAs(19~25 nucleotides),are expressed in almost all biota,including animals,viruses and plants.Their primary biological function is the regulation of gene expression at the post-transcriptional level,mainly via binding to the 3’-untranslated region of target genes.The binding of miRNAs to their target mRNAs may inhibit the translation or enhance the degradation of the target mRNAs.It has been reported that in human genome the expression of more than 60% genes are regulated by mi RNAs.Recently,more and more evidence showed miRNAs are involved in the regulation of tumor radiosensitivity,which maybe new potential clinical target for radiation sensitization.In order to reveal the relationship between miRNA and radiation lung injury,the effect of miRNA on radiation-induced lung injury and its mechanism in vitro was preliminarily discussed.In this study,we found that miR-26 b may play an important role in radiation-induced lung injury by referring to the relevant literature.We use human bronchial epithelial cells HBE as a cell model to interfere with the expression of miR-26 b after ionizing radiation,CCK8 was used to detect cell proliferation ability,flow cytometry analysis was used to the cell cycle distribution of HBE.The results: the expression level of miR-26 b in HBE cells is differentially expressed after ionizing radiation,and the expression of mi R-26 can significantly affect the proliferation of HBE cells and promote cell proliferation.Exposure to ionizing radiation after interfering HBE with miR-26 b inhibitor can affect the cell cycle distribution,which is blocked in the G2/M phase.Through bioinformatics analysis,CCND2 may be the target gene of miR-26 b.Mi R-26 b can be targeted to negatively regulate the expression of CCND2.Conclusion: miR-26 b is involved in the proliferation and release of HBE in human bronchial epithelial cells in vitro.The mechanism of the regulation of the sensitivity is related to the regulation of the cell cycle and other related proteins.However,further investigation is needed on the involved molecular mechanisms.