ITGA6通过PI3K/AKT信号通路调控腹壁子宫内膜异位症的机制研究OA

Objective To investigate the differential expression of integrin alpha-6(ITGA6)in abdominal wall en-dometriosis(AWE)tissues and its molecular mechanisms in regulating AWE.Methods 36 AWE lesions were designated as the experimental group,while 36 cases of normal endometrial tissues served as the controls.Differen-tial expression of ITGA6 between the two groups was assessed through immunohistochemical(IHC)staining.Hu-man ITGA6 gene-specific interference sequences were designed,synthesized,and packaged into lentiviral vectors to establish the Ishikawa cell line with ITGA6-knockdown.Similarly,the ITGA6-overexpression cell line was con-structed using the coding sequence(CDS)of the gene.Real-time PCR and Western blot were performed to detect changes in epithelial-mesenchymal transition(EMT)-related markers and angiogenesis-related indicators.Cell in-vasion and migration capabilities were assessed by Cell Scratch and Transwell assays.Furthermore,Western blot was conducted to profile PI3K/AKT pathway dynamics.Results Ectopic endometrial tissues exhibited a marked increase in the number of ITGA6-positive cells and their expression intensity compared to eutopic endometrium(each P<0.001).Compared with the NC group,the ITGA6-knockdown group showed significantly reduced ex-pression of N-cadherin,VEGF,and TGF-β1(all P<0.01),while E-cadherin expression was markedly increased(P<0.01).Concomitantly,the invasion and migration capacities of ITGA6-low expression were significantly im-paired(P<0.001 for both),accompanied by a marked reduction in AKT and phosphorylated AKT(p-AKT)levels(P<0.001).Conversely,overexpressing ITGA6 resulted in opposite effects.Conclusion ITGA6 modulates EMT and angiogenesis in Ishikawa cells via the PI3K/AKT signaling pathway,thereby enhancing cell invasion and migration capabilities,which contributes to the pathogenesis of AWE.