miR-101-3p inhibits EMT of gastric cancer cells and M2 polarization of macrophages by targeting Anxa2
10.3969/j.issn.1000-484X.2025.07.003
- VernacularTitle:miR-101-3p靶向调控Anxa2抑制胃癌细胞EMT和巨噬细胞M2极化
- Author:
Xiaotian ZHANG
1
;
Aojun WANG
1
;
Linqi MAO
1
;
Yu XU
1
Author Information
1. 山西医科大学汾阳学院医学检验系,汾阳 032200
- Publication Type:Journal Article
- Keywords:
Gastric cancer;
miR-101-3p;
Anxa2;
Macrophages;
M2 polarization;
EMT
- From:
Chinese Journal of Immunology
2025;41(7):1552-1558,1565
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the molecular mechanisms by which miR-101-3p inhibits epithelial-mesenchymal transition(EMT)of gastric cancer cells and M2 polarization of macrophages.Methods:Bioinformatics software was used to analyze the expres-sion of miR-101-3p in gastric cancer and its correlation with survival.Transwell and Western blot were performed to evaluate the effect of miR-101-3p and Anxa2 on the migration,invasion and EMT of gastric cancer cells.Human monocytes(THP-1)were co-cultured with transfected gastric cancer cells.Immunofluorescence and Western blot assays were performed to assess the impact of miR-101-3p and Anxa2 on the expression of M2 macrophage markers CD206 and arginase-1(Arg-1).Immunohistochemistry and Western blot were used to analyze the expression of Anxa2 in gastric cancer tissues and cells.Bioinformatics software,dual-luciferase reporter and West-ern blot were utilized to validate the target relationship between miR-101-3p and Anxa2.Results:Compared with adjacent tissues,the level of miR-101-3p in gastric cancer tissues was significantly reduced and positively correlated with survival.Additionally,the levels of miR-101-3p in gastric cancer cells were significantly lower than those in normal gastric mucosal cells(P<0.01).Overexpression of miR-101-3p in gastric cancer cells significantly reduced their migration and invasion capabilities.This was accompanied by a marked decrease in the expression of N-cadherin and vimentin,and a significant increase in the expression of E-cadherin.In the co-cultured system,overexpression of miR-101-3p in gastric cancer cells significantly inhibited macrophage M2 polarization(P<0.01).Compared with adjacent tissues,the level of Anxa2 was significantly elevated in gastric cancer tissues.Compared with normal gastric mucosal cells,Anxa2 levels were significantly higher in gastric cancer cells(P<0.01).Anxa2 was target gene of miR-101-3p.Overexpression of Anxa2 in gastric cancer cells significantly enhanced their migration and invasion capabilities.In the co-culture system,overexpres-sion of Anxa2 in gastric cancer cells markedly promoted macrophage M2 polarization(P<0.01).Overexpression of Anxa2 could re-verse the inhibitory effects of miR-101-3p on EMT of gastric cancer cells and M2 polarization of macrophages(P<0.01).Conclusion:miR-101-3p regulates Anxa2 to inhibit EMT of gastric cancer cells and M2 polarization of macrophages,thereby suppressing the migra-tion and invasion of gastric cancer cells.
