Effect and mechanism of cetuximab on cell proliferation of SW1990 and PANC-1 cells in pancreatic carcinoma
10.3969/j.issn.1005-1678.2017.07.065
- VernacularTitle:西妥昔单抗对胰腺癌SW1990、PANC-1细胞增殖的影响及其作用机制
- Author:
Yongqiang LV
;
Miao NIU
- Keywords:
cetuximab;
pancreatic carcinoma;
SW1990;
PANC-1;
proliferation;
mechanism
- From:
Chinese Journal of Biochemical Pharmaceutics
2017;37(7):168-170,173
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of cetuximab on the proliferation of pancreatic carcinoma cell lines SW1990 and PANC-1.Methods 100.0 μg/mL cetuximab added DMEM medium(cetuximab group), simple DEME medium as the control group, two groups of the pancreatic carcinoma cell lines SW1990 and PANC-1 were cultured, the SW1990 and PANC-1 were detected by MTT after cultured 12, 24, 48 h, the expression of epidermal growth factor receptor gene(EGFR-mRNA)and protein in two groups were detected by RT-PCR and Western-blot after 24 h;the cell cycle was detected by flow cytometry after 24 h, the activity of Wnt/ beta-catenin pathway was detected by double luciferase assay after 24 h.Results The OD of the cetuximab group of the SW1990 and PANC-1 cell lines proliferation were lower than the control group after 12, 24, 48 h (P<0.05);the OD of the cetuximab group of the SW1990 and PANC-1 cell lines proliferation in 24, 48 h was significantly decreased than 12 h (P<0.05);the proportion of G1 phase cells of the SW1990 and PANC-1 of the cetuximab group increased significantly than the control group (P<0.05), the proportion of S and G2 phase cells decreased significantly than the control group (P<0.05), the expression of the EGFR-mRNA and protein of the cetuximab group were lower than the control group (P<0.05),the TOP/FOP of the Wnt/beta-catenin pathways' activity of the cetuximab group was lower than that of the control group (P<0.05).Conclusion The proliferation of pancreatic carcinoma cell lines SW1990 and PANC-1 was significantly inhibited by cetuximab, which was mainly achieved by decreasing the activity of Wnt/beta-catenin pathway and the expression of EGFR-mRNA and protein.