The study of miR-26a regulates angiogenesis and its molecular mechanism in breast cancer through HGF/c-Met pathway
Objective To investigate the molecular mechanism of miR-26a in regulating breast cancer angiogenesis through hepato-cyte growth factor(HGF)/mesenchymal epithelial transition(c-Met)pathway.Method A total of 40 patients with breast cancer admit-ted to the hospital from January 2021 to March 2022 were included in the study.Breast cancer tissues and adjacent normal tissues were collected from all subjects to compare the relative expression levels of miR-26a and vascular endothelial growth factor A(VEGFA)mR-NA and microvessel density(MVD)in different breast tissues.In addition,the miR-26a mimics and inhibitors were transfected into breast cancer cells by LipofectamineTM2000 method,respectively,which were denoted as miR-26a transfection group and miR-26a in-hibition group,and the breast cancer cells without any treatment were used as negative control group.The expressions of HGF/c-Met pathway related proteins and their downstream target genes,phosphatidylinositol kinase 3(PI3K),protease B(AKT)and target of ra-pamycin(mTOR),were detected by PCR.Results The relative expression level of miR-26a in breast cancer tissues was lower than that in adjacent normal tissues.The relative expression level of VEGFA and MVD were higher than the normal tissues adjacent to cancer(P<0.05).The expression levels of HGF and p-c-Met/c-MET in miR-26a inhibition group were higher than the negative control group and miR-26a transfection group,the expression levels of HGF and P-c-Met/c-Met in the miR-26a transfection group were lower than those in the negative control group(P<0.05).The relative expression levels of PI3K,AKT and mTOR mRNA in miR-26a inhibi-tion group were higher than the negative control group and the miR-26a transfection group,the relative expressions of PI3K,AKT and mTOR mRNA in the miR-26a transfection group were lower than those in the negative control group(all P<0.05).Conclusion MiR-26a can further inhibit the occurrence and development of breast cancer by inhibiting the expression of PI3K,AKT and mTOR through inhibiting the HGF/c-Met pathway.
Breast cancerAngiogenesisMiR-26aHepatocyte growth factorC-mesenchymal epithelial transformationSigna-ling pathway
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