Abstract

Gastric cancer (GC) is one of the most lethal cancers worldwide. In this study, we aimed to explore the role of miR-129-5p, a newly identified miR-129 member, in GC cells as well as the potential mechanism of action. The results of reverse transcription - qualitative polymerase chain reaction (RT-qPCR) and Western Blot showed that miR-129 was downregulated in GC cells compared with normal ones. Using MTT, colony formation, wound healing assay, and a Transwell assay, we evaluated the proliferation, migration, and invasion abilities of transfected cells, and confirmed miR-129-5p as a tumor suppressor in GC. After a microarray analysis comparing different gene expressions in miR-129-5p transfected SGC-7901 cells, COL1A1 was selected for biggest fold-change and potential target of miR-129-5p predicted by TargetScan. Measured by RT-qPCR and Western blot, COL1A1 turned out to be upregulated in GC tissues and cells. We further confirmed the targeting relationship between miR-129-5p and COL1A1 by dual luciferase assay. By manipulating the expression of COL1A1 in SGC-7901 cells, cell proliferation, migration, and invasion were examined and the tumor-promoting function of COL1A1 was validated. Moreover, co-transfection of miR-129-5p mimics and COL1A1 attenuated the tumor-promoting effects induced by a single-transfection of COL1A1, and miR-129-5p inhibitor counteracted the tumor-suppressing effects of COL1A1 siRNA. Collectively, the data demonstrate the important functions of the miR-129-5p-COL1A1 axis in GC: miR-129-5p suppresses GC cell proliferation, migration, and invasion, by selectively inhibiting COL1A1. This study provides new therapeutic targets for the clinical treatment of GC.

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