癌症相关成纤维细胞（CAF）在预后不良的结肠癌（CC）患者中含量丰富。在此，探讨了CAF对CC生长和转移的分子调控机制。使用RT-qPCR、免疫印迹和免疫组织化学监测基因的表达。使用 CCK-8 和克隆形成测定发现细胞活力和增殖。使用伤口愈合和 Transwell 来探测细胞迁移和侵袭。 Co-IP 用于确定 AKT 和无名指蛋白 LIM 结构域相互作用 (RLIM) 之间的相互作用。建立体内小鼠皮下肿瘤模型和转移模型，进一步明确轴。结果表明，CAFs通过旁分泌软骨寡聚基质蛋白（COMP）促进CC细胞生长并激活PI3K/AKT通路。此外，RLIM促进CC细胞的生长，其蛋白稳定性受AKT通过磷酸化调节。此外，RLIM 促进早幼粒细胞白血病蛋白 (PML) 的泛素化和降解。体外和体内试验发现，PML过表达可抑制CC的生长和转移，而CAFs可增强CC的生长和转移。CAFs分泌的COMP通过调节RLIM/PML轴增强CC的生长和转移，为CC的生长和转移提供了新的潜在靶点。治愈 CC。© 2024 Journal of Gastroenterology and Hepatology Foundation 和 John Wiley

Cancer-associated fibroblasts (CAFs) are abundant in colon cancer (CC) patients with a poor prognosis. Here, the molecular regulatory mechanism of CAFs on CC growth and metastasis was explored.The genes' expression was monitored using RT-qPCR, immunoblotting, and immunohistochemistry. Cell viability and proliferation were found using CCK-8 and clone formation assays. The cell migration and invasion were probed using wound healing and Transwell. Co-IP was utilized for ascertaining the interaction between AKT and the ring finger protein, LIM domain interacting (RLIM). The in vivo murine subcutaneous tumor model and the metastasis model were built to further ascertain the axis.The result showed that CAFs motivate the growth and activate the PI3K/AKT pathway of CC cells via paracrine cartilage oligomeric matrix protein (COMP). Moreover, RLIM promoted the growth of CC cells, and its protein stability was regulated by AKT through its phosphorylation. Further, RLIM facilitated the ubiquitination and degradation of promyelocytic leukemia protein (PML). The in vitro and in vivo tests found that PML overexpression could inhibit CC's growth and metastasis, which were enhanced by CAFs.The COMP excreted from CAFs enhances the CC's growth and metastasis through regulating the RLIM/PML axis, supplying a new potential target for the cure of CC.© 2024 Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd.