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Establishment and characterization of an oxaliplatin-resistant hepatic cancer cell line
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作者 Ping Qiu Gang Chen +1 位作者 Yuhong Dai Hong Qiu 《Oncology and Translational Medicine》 2018年第2期48-53,共6页
Objective The aim of the current study was to establish an oxaliplatin-resistant hepatoma cell line(HepG2/OXA) and investigate the potential mechanisms of its drug resistance.Methods The hepatoma cell subline, HepG2/O... Objective The aim of the current study was to establish an oxaliplatin-resistant hepatoma cell line(HepG2/OXA) and investigate the potential mechanisms of its drug resistance.Methods The hepatoma cell subline, HepG2/OXA, resistant to oxaliplatin(OXA), was established from a parent cell line HepG2, by stepwise exposure to gradually increasing concentrations of OXA over a half-year period. Chemosenstivity of the cytotoxic drugs, OXA, cisplatin(CDDP), adriamycin(ADM), and 5-fuorouracil(5-FU), was determined in HepG2 and HepG2/OXA cells, by the Cell counting kit-8(CCK8) assay. Cell cycle distribution of HepG2 and HepG2/OXA cells was analyzed by Flow cytometry(FCM). The expression levels of several drug resistance-related proteins, such as P-glycoprotein(P-gp), multidrug resistant protein 1(MRP1), and excision repair-cross complementing 1(ERCC1) protein in the two cell lines were tested by the western blot assay.Results The IC50 of OXA in HepG2/OXA and HepG2 were 136.84 μmol/L and 23.86 μmol/L, respectively. The resistance index(RI) was 5.34. HepG2 was also demonstrated to be cross-resistant to other antitumor agents, such as 5-FU, ADM, and CDDP. The percentage of HepG2/OXA cells in the S phase was significantly decreased compared to HepG2 cells(25.58% ± 2.36% vs 14.37% ± 2.54%, P < 0.05), while the percentage of cells in the G0/G1 and G2/M phases showed no statistical difference(respectively 55.29% ± 4.98% vs 56.73% ± 4.56%, P > 0.05, and 24.63% ± 4.81% vs 28.26% ± 3.82%, P > 0.05). The ERCC1 was found to be over expressed in HepG2/OXA cells, while there was no difference in the expressions of P-gp and MRP1 between the multiple drug resistance(MDR) phenotype cell line and its parental cell line.Conclusion HepG2/OXA showed an MDR ability; the over expression of ERCC1 might be associated with the platinum resistance of the cells, but P-gp and MRP1 are not. 展开更多
关键词 房间 HEPG2 排队 癌症 P-GP OXA 蛋白质 细胞毒素
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Emodin regulating excision repair cross-complementation group 1 through fibroblast growth factor receptor 2 signaling 被引量:3
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作者 Gang Chen Hong Qiu +3 位作者 Shan-Dong Ke Shao-Ming Hu Shi-Ying Yu Sheng-Quan Zou 《World Journal of Gastroenterology》 SCIE CAS 2013年第16期2481-2491,共11页
AIM: To investigate the molecular mechanisms underlying the reversal effect of emodin on platinum resistance in hepatocellular carcinoma. METHODS: After the addition of 10 μmol/L emodin to HepG2/oxaliplatin (OXA) cel... AIM: To investigate the molecular mechanisms underlying the reversal effect of emodin on platinum resistance in hepatocellular carcinoma. METHODS: After the addition of 10 μmol/L emodin to HepG2/oxaliplatin (OXA) cells, the inhibition rate (IR), 50% inhibitory concentration (IC 50 ) and reversal index (IC 50 in experimental group/IC 50 in control group) were calculated. For HepG2, HepG2/OXA, HepG2/OXA/T, each cell line was divided into a control group, OXA group, OXA + fibroblast growth factor 7 (FGF7) group and OXA + emodin group, and the final concentrations of FGF7, emodin and OXA in each group were 5 ng/mL, 10 μg/mL and 10 μmol/L, respectively. Single-cell gel electrophoresis was conducted to detect DNA damage, and the fibroblast growth factor receptor 2 (FGFR2), phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) and excision repair cross-complementing gene 1 (ERCC1) protein expression levels in each group were examined by Western blotting. RESULTS: Compared with the IC50 of 120.78 μmol/L in HepG2/OXA cells, the IC 50 decreased to 39.65 μmol/L after treatment with 10 μmol/L emodin; thus, the reversal index was 3.05. Compared with the control group, the tail length and Olive tail length in the OXA group, OXA + FGF7 group and OXA + emodin group were significantly increased, and the differences were statistically significant (P < 0.01). The tail length and Olive tail length were lower in the OXA + FGF7 group than in the OXA group, and this difference was also statistically significant. Compared with the OXA + FGF7 group, the tail extent, the Olive tail moment and the percentage of tail DNA were significantly increased in the OXA + emodin group, and these differences were statistically significant (P < 0.01). In comparison with its parental cell line HepG2, the HepG2/OXA cells demonstrated significantly increased FGFR2, p-ERK1/2 and ERCC1 expression levels, whereas the expression of all three molecules was significantly inhibited in HepG2/ OXA/T cells, in which FGFR2 was silenced by FGFR2 shRNA. In the examined HepG2 cells, the FGFR2, p-ERK1/2 and ERCC1 expression levels demonstrated increasing trends in the OXA group and OXA + FGF7 group. Compared with the OXA group and OXA + FGF7 group, the FGFR2, p-ERK1/2, and ERCC1 expression levels were significantly lower in the OXA + emodin group, and these differences were statistically significant. In the HepG2/OXA/T cell line that was transfected with FGFR2 shRNA, the FGFR2, p-ERK1/2 and ERCC1 expression levels were significantly inhibited, but there were no significant differences in these expression levels among the OXA, OXA + FGF7 and OXA + emodin groups. CONCLUSION: Emodin markedly reversed OXA resistance by enhancing OXA DNA damage in HepG2/OXA cells, and the molecular mechanism was related to the inhibitory effect on ERCC1 expression being mediated by the FGFR2/ERK1/2 signaling pathway. 展开更多
关键词 Hepatocellular carcinoma EMODIN FIBROBLAST growth factor receptor 2 EXCISION repair crosscomplementation group 1 Platinum resistance EXTRACELLULAR SIGNAL-REGULATED KINASE
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