安徽医科大学学报2026，Vol.61Issue(1)：67-74,8.DOI:10.19405/j.cnki.issn1000-1492.2026.01.011
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
Mechanistic study on ITGA6 regulation of abdominal wall endometriosis via the PI3K/AKT signaling pathway
摘要
Abstract
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.关键词
整合素α6/子宫内膜异位症/上皮-间质转化/血管生成/细胞黏附Key words
integrin alpha-6/endometriosis/epithelial-mesenchymal transition/angiogenesis/cell adhesion分类
医药卫生引用本文复制引用
顾蓉,黄海良,王心蕊,李涵璐,刘开江,朱颍..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[J].安徽医科大学学报,2026,61(1):67-74,8.基金项目
国家自然科学基金项目(编号:82371652、82371658) （编号:82371652、82371658）
安徽省高校自然科学研究项目(编号:2023AH053331) National Natural Science Foundation of China(Nos.82371652,82371658) （编号:2023AH053331）
Natural Science Research Project of Anhui Educational Committee(No.2023AH053331) （No.2023AH053331）
