RESUMO
Objective To investigate the effect of transcription factor atonal homolog 8(ATOH8)and miR-125a on lung cancer progres-sion and its potential upstream regulatory mechanism.Methods ATOH8 expression levels in lung adenocarcinoma and their correlation with survival rate were analyzed using the online database UALCAN.miR-125a expression levels in lung adenocarcinoma and their rela-tionship with lung cancer progression were also analyzed using the UALCAN database.Total RNA extracted from lung adenocarcinoma tumors and adjacent normal tissues was used to perform real-time PCR in order to analyze these expression levels.The effect of ATOH8 overexpression on lung adenocarcinoma cell survival was detected using CCK-8 assays.A miR-125a mimic and inhibitor were transfected into lung adenocarcinoma cells,and ATOH8 expression levels were detected by real-time PCR and Western blotting.Results Statistical analysis showed that ATOH8 was significantly down-regulated in lung adenocarcinoma tissues(P＜0.01)and ATOH8 overexpression significantly reduced the survival of lung adenocarcinoma cells(P＜0.05).Furthermore,the five-year survival rate of patients with high ATOH8 expression levels was significantly increased(P＜0.05).miR-125a can bind to the 3'untranslated regions(3'UTR)of ATOH8 and significantly inhibit its expression levels(P＜0.05).However,miR-125a was significantly up-regulated in lung adenocarcinoma patients with a history of smoking,middle and advanced stage,and lymphatic metastasis(P＜0.05).Conclusion ATOH8,as a poten-tial tumor suppressor gene,can inhibit lung adenocarcinoma cell survival and affect the five-year survival rate of patients.miR-125a expression levels were closely related to smoking history,tumor stage,and lymphatic metastasis.Overall,the inhibiting effect of miR-125a against ATOH8 is a potential reason for abnormal ATOH8 expression in lung adenocarcinoma.