〔Abstract〕 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-阝1（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 （all 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.