@Article{096504017X14879366402279,
AUTHOR = {Xiaoyu Wu, Jin Zhou, Zhenfeng Wu, Che Chen, Jiayun Liu, Guannan Wu, Jing Zhai, Fukun Liu, Gang Li},
TITLE = {miR-101-3p Suppresses HOX Transcript Antisense RNA (HOTAIR)-Induced  Proliferation and Invasion Through Directly Targeting SRF  in Gastric Carcinoma Cells},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {8},
PAGES = {1383--1390},
URL = {http://www.techscience.com/or/v25n8/56923},
ISSN = {1555-3906},
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.},
DOI = {10.3727/096504017X14879366402279}
}