Exosomal miR-502-5p suppresses the progression of gastric cancer by repressing angiogenesis through the Wnt/β-catenin pathway

被引:2
作者
Zhou, Yanwu [1 ]
Li, Rong [2 ]
机构
[1] Cent South Univ, Xiangya Hosp, Dept Thorac Surg, Changsha 410011, Peoples R China
[2] Cent South Univ, Xiangya Hosp 2, Dept Gastroenterol, 139 Renmin Middle Rd, Changsha 410011, Peoples R China
基金
中国国家自然科学基金;
关键词
Angiogenesis; Exosomes; Gastric cancer; MiR-502-5p; Wnt/beta-catenin; COLORECTAL-CANCER; DOWN-REGULATION; BREAST-CANCER; METASTASIS; ONCOGENES; MICRORNAS;
D O I
10.1007/s11845-024-03789-0
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
BackgroundGastric cancer (GC) is a significant global health concern, ranking as the fifth most common cancer and the third leading cause of cancer-related deaths. The role of miR-502-5p in various cancers has been studied, but its specific impact on gastric cancer through exosomes is not well understood. This study aimed to investigate the role and mechanism of exosome-derived miR-502-5p in gastric cancer.MethodsDifferential expression of miR-502-5p in tissues or serum of GC patients was determined using qRT-PCR. The impact of miR-502-5p on cell proliferation, migration, and invasion was assessed through in vitro and in vivo experiments. The potential of exosome-miR-502-5p to inhibit metastatic ability was also explored by using vivo and vitro assay. Furthermore, the underlying mechanism of miR-502-5p in gastric cancer was investigated using western blotting.ResultsIt was found that miR-502-5p suppressed the proliferation, migration, and invasion of gastric cancer cells. Exosome-miR-502-5p expression was negatively linked to metastatic ability and demonstrated inhibition of metastasis in vitro and in vivo. Additionally, miR-502-5p appeared to inhibit angiogenesis through the Wnt/beta-catenin pathway in gastric cancer.ConclusionsExosomal miR-502-5p acts as a suppressor in the development and progression of gastric cancer, suggesting its potential as a target for anti-cancer therapy or as a diagnostic biomarker.
引用
收藏
页码:2681 / 2694
页数:14
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