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CircRBMS3 promotes gastric cancer tumorigenesis by regulating miR‐153–SNAI1 axis
Author(s) -
Li Guangyan,
Xue Minghui,
Yang Fang,
Jin Yuhong,
Fan Yingying,
Li Wei
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.27122
Subject(s) - snai1 , carcinogenesis , biology , gene silencing , cancer , cancer research , malignancy , downregulation and upregulation , microrna , metastasis , epithelial–mesenchymal transition , gene , genetics
Gastric cancer (GC) is one of the leading causes of cancer‐related death worldwide. Mounting evidence showed that circular RNAs (circRNAs) play critical roles in human malignancy. However, the knowledge about circRNAs in GC is still unclear. In the current study, high throughput microarray assay showed that circRBMS3 was upregulated in GC tissues, which was further confirmed by quantitative reverse transcription polymerase chain reaction. Correlation analysis revealed that high circRBMS3 expression was associated with advanced TNM stage, depth of invasion, and lymph‐node metastasis. Kaplan–Meier analysis indicated that GC patients with high circRBMS3 expression have a poor overall survival (OS). Function assays showed that circRBMS3 silencing reduced GC cells proliferation and invasion in vitro, and inhibited the tumor growth in vivo. Mechanistically, we found that miR‐153 could act as a target of circRBMS3. Subsequently, we showed that circRBMS3 promoted snail family zinc finger 1 (SNAI1) expression via inhibiting miR‐153 in GC cells. Collectively, these results suggested that circRBMS3 promoted GC cells proliferation and invasion via regulating miR‐153/SNAI1 axis.