Changhe Jia1, Yanrui Zhang1, Yi Xie2, Ying Ren3, Haihui Zhang1, Yinglei Zhou1, Ning Gao1, Songze Ding1, Shuangyin Han1. 1. Department of Gastroenterology, Henan Provincial People's Hospital, The People's Hospital of Zhengzhou University , Zhengzhou , Henan Province , 450000 , P. R. China. 2. Department of Gastrointestinal Surgery, Henan Provincial People's Hospital, The People's Hospital of Zhengzhou University , Zhengzhou , Henan Province , 450000 , P. R. China. 3. Department of Pathology, Henan Provincial People's Hospital, The People's Hospital of Zhengzhou University , Zhengzhou , Henan Province , 450000 , P. R. China.
Abstract
Background: The role of miR-200a-3p in gastric cancer (GC) remain unclear. Materials and methods: miR-200a-3p expression in 65 paired GC and adjacent tissues (AT) were evaluated by quantitative real-time PCR (qRT-PCR) and Western blot. Cell proliferation, cell cycle, and cell migration were assessed by cell growth counting assay, cell cycle analysis, and transwell assay, respectively. The target of miR-200a-3p was analyzed by dual-luciferase reporter assay. Results: miR-200a-3p in GC tissues was significantly reduced compared with AT. miR-200a-3p expression was closely associated with clinicopathological features (P < .05). SGC-7901 cell line demonstrated the lowest level of miR-200a-3p. Cell proliferation and colony formation was significantly inhibited by miR-200a-3p overexpression, but increased by miR-200a-3p knockdown (P < .05). miR-200a-3p upregulation increased the G1/S cell ratio. The 3'-UTR of KLF12 directly interacted with miR-200a-3p. Furthermore, increased levels of KLF12 expression was detected in GC tissues. A correlation analysis suggested a negatively correlation between miR-200a-3p and KLF12 mRNA expressions. Conclusion: miR-200a-3p was down-regulated in GC tissues and was correlated with clinicopathological features. miR-200a-3p overexpression inhibits GC cell proliferation, cell cycle, and cell migration. Furthermore, miR-200a-3p might act as a tumor suppressor in GC by targeting KLF12.
Background: The role of miR-200a-3p in gastric cancer (GC) remain unclear. Materials and methods: miR-200a-3p expression in 65 paired GC and adjacent tissues (AT) were evaluated by quantitative real-time PCR (qRT-PCR) and Western blot. Cell proliferation, cell cycle, and cell migration were assessed by cell growth counting assay, cell cycle analysis, and transwell assay, respectively. The target of miR-200a-3p was analyzed by dual-luciferase reporter assay. Results:miR-200a-3p in GC tissues was significantly reduced compared with AT. miR-200a-3p expression was closely associated with clinicopathological features (P < .05). SGC-7901 cell line demonstrated the lowest level of miR-200a-3p. Cell proliferation and colony formation was significantly inhibited by miR-200a-3p overexpression, but increased by miR-200a-3p knockdown (P < .05). miR-200a-3p upregulation increased the G1/S cell ratio. The 3'-UTR of KLF12 directly interacted with miR-200a-3p. Furthermore, increased levels of KLF12 expression was detected in GC tissues. A correlation analysis suggested a negatively correlation between miR-200a-3p and KLF12 mRNA expressions. Conclusion:miR-200a-3p was down-regulated in GC tissues and was correlated with clinicopathological features. miR-200a-3p overexpression inhibits GC cell proliferation, cell cycle, and cell migration. Furthermore, miR-200a-3p might act as a tumor suppressor in GC by targeting KLF12.