HCA-7 Colony 29

P-Cadherin Knockout Accelerates IEC Wound Healing by Modulating Cell-Matrix Adhesion and Cell Spreading

Inflammatory bowel diseases (IBD) cause recurrent intestinal inflammation, disrupting epithelial homeostasis and potentially leading to colitis-associated colon cancer (CAC). P-cadherin, an adhesion protein upregulated in inflamed mucosa, may play a role in intestinal inflammation and CAC. Naydenov et al. investigated P-cadherin's roles in these processes.

They investigated the role of P-cadherin in modulating intestinal epithelial cell (IEC) migration using HCA-7 Colony 29 (referred hereafter as HCA-7) - and SK-CO15 cells, well-differentiated human colonic carcinoma cell lines. CRISPR-Cas9 was used to knockout P-cadherin in these cell lines. The loss of P-cadherin did not significantly affect cell proliferation but significantly enhanced collective IEC migration in wound healing models (Fig. 1C-F). Live imaging of wounded HCA-7 monolayers showed higher migration velocity in P-cadherin knockout cells compared to controls (Fig. 2A). Individual cell migration analysis revealed increased migrated distance and speed but decreased directionality in P-cadherin-deficient cells (Fig. 2B-E). These findings suggest that P-cadherin directly affects cell motility, crucial for wound healing, rather than indirectly influencing it through junctional remodeling.

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