Colorectal fibroblasts promote malignant phenotype of colorectal cancer cells by activating the ERK signaling pathway
10.12122/j.issn.1673-4254.2024.10.04
- VernacularTitle:结直肠成纤维细胞通过激活ERK信号通路促进结直肠癌细胞的恶性生物学行为
- Author:
Xueyan XI
1
;
Ting DENG
;
Boyu DU
Author Information
1. 湖北医药学院基础医学院免疫教研室,湖北 十堰 442000
- Keywords:
fibroblasts;
colorectal cancer;
stemness;
ERK
- From:
Journal of Southern Medical University
2024;44(10):1866-1873
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of human colorectal fibroblast(CCD-18Co)-conditioned medium(CCD18-Co-CM)on biological behaviors of colorectal cancer(CRC)cells and explore the possible molecular mechanisms.Methods Real-time cellular analysis(RTCA),clone formation assay and wound healing assay were used to analyze the changes in proliferation,clone formation,and migration abilities of CRC cell lines HCT116 and Caco-2 treated with CCD18-Co-CM.Western blotting was used to detect the changes in ATK,ERK and STAT3 signaling pathways in the CRC cells activated by CCD18-Co-CM.The effect of CCD18-Co-CM on spheroidization ability of the cells was assessed with sphere-formation assay,and the changes in expressions of CRC stemness markers were detected using RT-PCR.Results CCD-18Co-CM significantly promoted proliferation,colony formation,and migration of HCT116 and Caco-2 cells,enhanced sphere-forming ability and expressions of CRC stemness markers,and increased ERK phosphorylation in the cells.Treatment with SCH772984 effectively inhibited CCD-18Co-CM-induced ERK signaling pathway activation,suppressed the malignant phenotype,and lowered the sphere-forming ability and expression of stemness markers of the two CRC cells.Conclusion Colorectal fibroblasts promote malignant phenotype of CRC cells by activating the ERK signaling pathway.