miR-200a-3p plays tumor suppressor roles in gastric cancer cells by targeting KLF12

The role of miR-200a-3p in gastric cancer (GC) remain unclear. 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, cel...

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Veröffentlicht in:Artificial cells, nanomedicine, and biotechnology nanomedicine, and biotechnology, 2019-12, Vol.47 (1), p.3697-3703
Hauptverfasser: Jia, Changhe, Zhang, Yanrui, Xie, Yi, Ren, Ying, Zhang, Haihui, Zhou, Yinglei, Gao, Ning, Ding, Songze, Han, Shuangyin
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Sprache:eng
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Zusammenfassung:The role of miR-200a-3p in gastric cancer (GC) remain unclear. 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. 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. 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.
ISSN:2169-141X
DOI:10.1080/21691401.2019.1594857