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Low expression of GATA3 promotes cell proliferation and metastasis in gastric cancer

Authors Wei S, Zhong L, Wang X, Zhang W

Received 1 August 2017

Accepted for publication 5 September 2017

Published 7 December 2017 Volume 2017:9 Pages 769—780

DOI https://doi.org/10.2147/CMAR.S147973

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 2

Editor who approved publication: Dr Kenan Onel


Shuangqin Wei,1 Liang Zhong,2 Xiaoping Wang,1 Wenju Zhang3

1Department of Gastroenterology, Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital, 2Department of Gastroenterology, Huashan Hospital, Fudan University, 3School of Life Science, Shanghai University, Shanghai, People’s Republic of China

Abstract:
GATA3, a member of the GATA zinc finger transcription factor family, has been widely investigated for its role in cancer. Although a recent report has found that GATA3 is downregulated in gastric cancer (GC), the detailed mechanism of GATA3 in GC is still unknown. Here, we investigated whether GATA3 was downregulated in GC patients’ tissue samples and cell lines using quantitative real time polymerase chain reaction and Western blotting. In addition, we conducted several functional experiments to investigate the effect of GATA3 in GC, including cell proliferation, metastasis and epithelial–mesenchymal transition (EMT). The results showed that GATA3 was downregulated in GC tissue samples and cells. Moreover, the expression of GATA3 was associated with tumor size, stage and metastasis. Restoration of GATA3 levels suppressed GC cell proliferation, migration and invasion. Furthermore, chromatin immunoprecipitation and luciferase reporter assay also revealed that GATA3 transcriptionally regulated ZEB1, thereby suppressing EMT. All these findings suggest that GATA3 serves as an oncogene in GC development.

Keywords: invasion, EMT, ZEB1

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