Curcumin reversal multidrug resistance through downregulation of STAT3 signaling in colon cancer cell lines resistant to oxaliplatin
10.3969/j.issn.1000-484X.2015.08.012
- VernacularTitle:姜黄素通过抑制STAT3通路调控人结肠癌耐奥沙利铂细胞株的耐药性
- Author:
Kunming WEN
;
Min LENG
;
Jiaping CHENG
;
Zhengquan CHEN
;
Yilin CHENG
;
Qingliang ZENG
- Publication Type:Journal Article
- Keywords:
Colon cancer;
Multi-drug resistance;
Curcumin;
STAT3 signaling pathway
- From:
Chinese Journal of Immunology
2015;(8):1056-1059
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the reversal multidrug resistance effects of curcumin on human colorectal cancer cell lines resistant to oxaliplatin( SW620/OxR) and whether its mechanism was involved in downregulation of STAT3 signaling.Methods: The IC50 value(50%cell growth inhibitory concentrations) of curcumin to SW620/OxR cell lines was obtained by WST-1 reagent,which was one kind of cell proliferation assay.Later experiments included in the experimental group and the control group.In the experimental group,SW620/OxR cell lines were exposed to the previous experiment IC50 concentrations of curcumin plus 2 μmol/L oxaliplatin for 48 h,while in the control group,SW620/OxR cell lines were cultured in medium containing in 2μmol/L oxaliplatin.In the two groups:apoptosis was detected by flow cytometry;the protein expression levels of phosphorylated STAT3(P-STAT3) and P-gp were disclosed by Western blot.Results:The IC50 value of curcumin to SW620/OxR cell lines was 18.9 μmol/L.The apoptosis rate of cells in the control group and the experimental group were respectively ( 5.08 ±1.82 )% and ( 30.69 ±2.94 )%, the apoptosis rate of the experimental group was significantly higher than that of the control group ( P<0.05 ) .The protein expression levels of phosphorylated STAT3(P-STAT3) and P-gp in the experimental group was significantly lower than that in the control group(P<0.05).Conclusion:Curcumin can reverse drug resistance in colorectal cancer cell lines resistant to oxaliplatin, its effect may be associated with downregulation of STAT3 signaling pathways.
