CircRNA-ABCB10 promotes gastric cancer progression by sponging miR-1915-3p to upregulate RaC1

被引:5
作者
Liu, Junhui [1 ]
Qiu, Guanglin [2 ]
Wang, Haijiang [2 ]
Li, Na [1 ]
Liao, Xinhua [2 ]
机构
[1] Xi An Jiao Tong Univ, Dept Clin Lab, Affiliated Hosp 1, Xian 710061, Shaanxi, Peoples R China
[2] Xi An Jiao Tong Univ, Dept Gen Surg, Affiliated Hosp 1, 277 Yanta West Rd, Xian 710061, Shaanxi, Peoples R China
关键词
Circ-ABCB10; Gastric cancer; miR-1915-3p; Rac1; Tumorigenesis; CIRCULAR RNA; BREAST-CANCER; RESISTANCE; EXPRESSION; BIOMARKER; CELLS;
D O I
10.1016/j.dld.2021.12.001
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background: Gastric cancer (GC) is a common malignant tumor of the digestive system. Increasing reports have demonstrated the crucial roles of circRNAs in tumorigenesis and progression of GC. Methods: The relative expression of circ-ABCB10 in GC tissues and cell lines was detected by qRT-PCR. A series of in vitro assays and a xenograft model in vivo were applied to explore the function of circ-ABCB10 in GC cells. Results: Circ-ABCB10 expression was upregulated in GC tissues and cell lines and positively correlated with poor survival of GC patients. Circ-ABCB10 downregulation decreased cell viability, inhibited cell growth, invasion, and migration, while promoted cell apoptosis of GC cell lines SGC-7901 and MKN-48. Circ-ABCB10 could upregulate Rac1 expression by directly sponging miR-1915-3p. Rescue experiments revealed that miR-1915-3p inhibitor obviously reversed the inhibitory effect of si-circ-ABCB10, and Rac1 overexpression obviously reversed the inhibitory effect of miR-1915-3p mimics on cell growth, invasion, migration, apoptosis, and cell cycle progression. Moreover, si-circ-ABCB10 effectively inhibited tumor growth in a xenograft model. Conclusions: Our study revealed that circ-ABCB10 promoted GC progression via targeting the miR-1915-3p/Rac1 axis, and circ-ABCB10 might be a potential target for GC diagnosis and treatment. (C) 2021 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:896 / 904
页数:9
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