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miR‐188‐5p emerges as an oncomiRNA to promote gastric cancer cell proliferation and migration via upregulation of SALL4
Author(s) -
Wang Mei,
Qiu Rong,
Gong Zheng,
Zhao Xinxin,
Wang Tingting,
Zhou Lulu,
Lu Weiwei,
Shen Bo,
Zhu Wei,
Xu Wenrong
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28764
Subject(s) - downregulation and upregulation , cell growth , microbiology and biotechnology , cancer research , cancer , chemistry , biology , biochemistry , genetics , gene
MicroRNAs (miRNAs) play pivotal roles in modulating key biological processes in gastric cancer (GC). As a newly identified miRNA, the function and potential mechanism of miR‐188‐5p in GC has not been thoroughly elucidated. Here, quantitative real‐time polymerase chain reaction detection showed abnormally higher expression of miR‐188‐5p in GC cells and tissues. Gain‐of‐function analysis in vitro showed that miR‐188‐5p promoted GC cell proliferation and migration, while loss‐of‐function studies showed the reverse. Targetscan has predicted that phosphatase and tensin homolog (PTEN) was a potential target gene of miR‐188‐5p. miR‐188‐5p suppressed PTEN messenger RNA and protein expression and activated downstream AKT/mTOR signaling in GC cells, but luciferase reporter analysis showed that PTEN was not regulated by miR‐188‐5p via the 3′ untranslated region. Furthermore, we observed that miR‐188‐5p overexpression promoted Sal‐like protein 4 (SALL4) protein expression, cellular nuclear translocation, and transcription. Knockdown of SALL4 eliminated the effect of miR‐188‐5p in GC cells as well as suppression of PTEN. Taken together, our results demonstrate that miR‐188‐5p promotes GC cell proliferation and migration while suppressing tumor suppressor gene PTEN expression via transcriptional upregulation of oncogene SALL4. We conclude that miR‐188‐5p acts as an oncomiRNA in GC and may be a promising therapeutic target for GC.