MicroRNA-513b-5p inhibits epithelial mesenchymal transition of colon cancer stem cells through IL-6/STAT3 signaling pathway

被引:0
|
作者
Zhang, Zefeng [1 ,2 ]
Sha, Weihong [1 ,2 ]
机构
[1] Southern Med Univ, Guangdong Prov Peoples Hosp, Guangdong Acad Med Sci, Dept Gastroenterol, Guangzhou 510080, Guangdong, Peoples R China
[2] Southern Med Univ, Guangdong Prov Peoples Hosp, Guangdong Acad Med Sci, Digest Endoscopy Ctr, Guangzhou 510080, Guangdong, Peoples R China
关键词
miR-513b-5p; IL-6/STAT3; Colon cancer stem cells; EMT; Metastasis; COLORECTAL-CANCER; DOWN-REGULATION; IN-VITRO; IDENTIFICATION; PROMOTES; MARKERS; SUBPOPULATION; EXPRESSION; CULTURE; CD166;
D O I
10.1007/s12672-024-01137-3
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
ObjectiveTo reveal the mechanisms by which miR-513b-5p inhibits metastasis of colon cancer stem cells (CCSCs) through IL-6/STAT3 in HCT116 cells.MethodsSphere formation media and magnetic cell sorting were used to enrich and screen CCSCs. We used a colony formation assay, cell proliferation and viability assays, and a nude mouse transplantation tumor assay to identify CCSCs. ELISA was performed to identify IL-6 in the cell culture medium, and the growth, viability, wound healing, and transwell migration of distinct cell groups were compared to differentiate them. Dual-luciferase reporter assay, RT-PCR, and/or Western Blot analysis were conducted to determine the correlation between them.ResultsCD133+CD44+ HCT116 cells were shown to have higher cloning efficiency, greater proliferation ability and viability, and stronger tumorigenicity. A dual-luciferase reporter assay revealed that miR-513b-5p negatively affected STAT3 expression. RT-PCR and/or Western Blot analysis suggested that miR-513b-5p negatively affected STAT3 and Vimentin, while positively affecting E-cadherin expression. The STAT3 overexpression vector + miR-513b-5p inhibitor cell group had the highest efficiency, greatest proliferation ability and viability, and the highest IL-6 level in the experiments.ConclusionsMir-513b-5p inhibited the epithelial-mesenchymal transition (EMT) of CCSCs through IL-6/STAT3. This potential mechanism may provide a new therapeutic target for colon cancer.
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页数:14
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