Open Access

ARTICLE

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

Xiaoyu Wu^*1, Jin Zhou^†1, Zhenfeng Wu^*, Che Chen^*, Jiayun Liu^*, Guannan Wu^*, Jing Zhai^*, Fukun Liu^*, Gang Li^‡

* Department of Surgical Oncology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, P.R. China
† Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, P.R. China
‡ Department of General Surgery, Jiangsu Cancer Hospital, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, P.R. China
1 These authors provided equal contribution to this work.

Oncology Research 2017, 25(8), 1383-1390. https://doi.org/10.3727/096504017X14879366402279

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 wellcharacterized 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 HOTAIRinduced proliferation and invasion through directly targeting SRF in gastric carcinoma cells.

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Keywords

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