Yinhua Liu1, Jiaping Li2, Sufeng Wang1, Hong Song1, Tao Yu3,4. 1. Department of Pathology, Wannan Medical College First Affiliated Hospital, Yijishan Hospital , Wuhu, Anhui Province, China. 2. Department of Cardiothoracic Surgery, Wannan Medical College First Affiliated Hospital, Yijishan Hospital , Wuhu, Anhui Province, China. 3. Department of Neurosurgical Intensive Care Unit, Wannan Medical College First Affiliated Hospital, Yijishan Hospital , Wuhu, Anhui Province, China. 4. Research Center for Functional Maintenance and Reconstruction of Viscera, Wannan Medical College First Affiliated Hospital, Yijishan Hospital , Wuhu, Anhui Province, China.
Abstract
BACKGROUND: MicroRNAs (miRNAs) as the subtype of non-coding RNAs are revealed to be crucial players in cellular activities. It has been reported that miR-3619-5p functions as a tumor inhibitor in several cancers. However, the connection between miR-3619-5p and stomach adenocarcinoma (STAD) remains to be discovered. AIM OF THE STUDY: The purpose of the study is to figure out the role and molecular regulation mechanism of miR-3619-5p in STAD. METHODS: The expression of miR-3619-5p was evaluated via qRT-PCR analysis. Gain-of-function experiments demonstrated the effects of miR-3619-5p on cellular functions. The upper-stream transcription factor STAT4 and downstream target gene TBC1D10B of miR-3619-5p were identified by bioinformatic analysis. The binding and interaction between the indicated molecules were verified by RNA pull-down and luciferase reporter assays. RESULTS: The expression of miR-3619-5p was prominently down-regulated in STAD cells and tissues. MiR-3619-5p suppresses cell proliferation, migration, invasion and tumor growth in STAD. Further, STAT4 bound with miR-3619-5p promoter and inhibited its transcription. MiR-3619-5p was also recognized to modulate STAD progression through the regulation of downstream target gene TBC1D10B. CONCLUSION: STAT4-mediated miR-3619-5p controls STAD carcinogenesis and progression through modulating TBC1D10B expression, which may provide a novel insight for researching the STAD-related molecular mechanism.
BACKGROUND: MicroRNAs (miRNAs) as the subtype of non-coding RNAs are revealed to be crucial players in cellular activities. It has been reported that miR-3619-5p functions as a tumor inhibitor in several cancers. However, the connection between miR-3619-5p and stomach adenocarcinoma (STAD) remains to be discovered. AIM OF THE STUDY: The purpose of the study is to figure out the role and molecular regulation mechanism of miR-3619-5p in STAD. METHODS: The expression of miR-3619-5p was evaluated via qRT-PCR analysis. Gain-of-function experiments demonstrated the effects of miR-3619-5p on cellular functions. The upper-stream transcription factor STAT4 and downstream target gene TBC1D10B of miR-3619-5p were identified by bioinformatic analysis. The binding and interaction between the indicated molecules were verified by RNA pull-down and luciferase reporter assays. RESULTS: The expression of miR-3619-5p was prominently down-regulated in STAD cells and tissues. MiR-3619-5p suppresses cell proliferation, migration, invasion and tumor growth in STAD. Further, STAT4 bound with miR-3619-5p promoter and inhibited its transcription. MiR-3619-5p was also recognized to modulate STAD progression through the regulation of downstream target gene TBC1D10B. CONCLUSION:STAT4-mediated miR-3619-5p controls STAD carcinogenesis and progression through modulating TBC1D10B expression, which may provide a novel insight for researching the STAD-related molecular mechanism.