Overexpression of amphiregulin promotes the growth of mouse colon carcinoma CT26 cells in vivo / 肿瘤

ABSTRACT

Objective: To investigate the effect of epidermal growth factoramphiregulin (AREG) on the growth of mouse colon carcinoma CT26cells and its related mechanisms.Methods: The protein expression level of AREG in different mouse cancer cells was detected by ELISA. Mouse colon carcinoma CT26 cells, melanoma B16 cellsand hepatocellular carcinoma LPC-Akt cells were transfected with the recombinant lentiviralplasmid carrying AREG gene, while the ones transfected with empty plasmid were used asthe negative controls. After AREG overexpression, the cell proliferation, colony-formingabilities and cell cycle progression in vitro were detected by MTT, colony-forming assay andFCM, respectively. After the homograft mouse model of CT26 cells was constructed, thegrowth of homograft tumor was observed, the distribution of immune cells in tumor tissueswas detected by FCM, furthermore the expression of chemokine was detected by real-timefluorescent quantitative PCR.Results: The levels of AREG expression were relatively low in mouse colon carcinoma CT26cells, melanoma B16 cells and hepatoma LPC-Akt cells. AREG overexpression did notmarkedly affect the proliferation, colony-forming abilities and cell cycle progression of thesethree types of tumor cells in vitro (all P > 0.05). However, in the homograft mouse model ofCT26 cells, AREG overexpression significantly promoted the growth of tumor cells in vivo (P <0.01), decreased the percentage of CD8+ T cells (P < 0.05), and reduced the mRNA level ofCC chemokine 5 ligand (CCL5) (P < 0.05) which was related to CD8+ T cell recruitment.Conclusion: AREG promotes the growth of mouse colon carcinoma CT26 cells in vivo . AREGmay affect the tumor microenvironment by regulating the production of chemokine which isrelated to CD8+ T cell recruitment.