miR-101-3p Suppresses HOX Transcript Antisense RNA (HOTAIR)-Induced Proliferation and Invasion Through Directly Targeting SRF in Gastric Carcinoma Cells.

Abstract	miR-101-3p has been identified as a tumor suppressor in several cancers, but its exact role in gastric adenocarcinoma is still largely unknown. In this study, we found that, compared with the RGM-1 human normal gastric epithelial cells, miR-101-3p was significantly downregulated in all six human gastric adenocarcinoma cell lines, including BGC-823, MNK-45, MGC-803, SGC-7901, AGS, and HGC-27. Overexpression of miR-101-3p suppressed both the proliferation and invasion of AGS gastric adenocarcinoma cells, and knockdown of miR-101-3p displayed the opposite effect. In addition, miR-101-3p could directly target and suppress the expression of the serum response factor (SRF) gene, which is a transcription factor of HOTAIR, a well-characterized tumor promoter lncRNA. miR-101-3p negatively regulated SRF-mediated transcription of HOTAIR. Moreover, silencing of either SRF or HOTAIR could counteract the promotion of gastric adenocarcinoma cell proliferation and invasion by miR-101-3p inhibition. Our findings indicate that miR-101-3p suppresses HOTAIR-induced proliferation and invasion through directly targeting SRF in gastric carcinoma cells.
Authors	Xiaoyu Wu, Jin Zhou, Zhenfeng Wu, Che Chen, Jiayun Liu, Guannan Wu, Jing Zhai, Fukun Liu, Gang Li
Journal	Oncology research (Oncol Res) Vol. 25 Issue 8 Pg. 1383-1390 (Sep 21 2017) ISSN: 1555-3906 [Electronic] United States
PMID	28251884 (Publication Type: Journal Article)
Chemical References	HOTAIR long untranslated RNA, human MIRN101 microRNA, human MicroRNAs RNA, Long Noncoding SRF protein, human Serum Response Factor
Topics	Adenocarcinoma (genetics, metabolism, pathology) Cell Line, Tumor Cell Proliferation (genetics) Down-Regulation Humans MicroRNAs (genetics, metabolism) Neoplasm Invasiveness RNA, Long Noncoding (biosynthesis, genetics, metabolism) Serum Response Factor (genetics, metabolism) Stomach Neoplasms (genetics, metabolism, pathology) Transfection

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