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目的:探讨耐药基因MDR1(P-gp)和ABCG2在Hep-2细胞耐药中的作用。方法:应用流式细胞仪检测MDR1和ABCG2抑制剂对于Hep-2喉癌细胞株积聚和外排抗肿瘤药物功能的影响,以及MDR1和ABCG2抑制剂对于Hep-2喉癌细胞株增敏作用的影响。结果:ABCG2抑制剂FTC在Hep-2细胞对Mitoxantrone吸收、外排检测实验中与对照组比较,差异有统计学意义;P-gp在该实验中与对照组差异无统计学意义;当抗肿瘤药物为Mitoxantrone及Cisplatin时,P-gp及ABCG2拮抗剂的加入对Hep-2细胞活力检测与对照组比较,差异无统计学意义;当抗肿瘤药为Doxorubicin时,FTC、P-gp单独作用对Hep-2细胞活力影响与对照组比较差异无统计学意义;而当FTC+P-gp时,对Hep-2细胞活力影响与对照组比较差异有统计学意义(P<0.05);当抗肿瘤药为5-FU时,P-gp对Hep-2细胞活力影响相比对照组差异有统计学意义(P<0.05),而FTC对该药耐药几乎无任何影响,FTC+P-gp也无效;当抗肿瘤药为Paclitaxel时,P-gp对Hep-2细胞活力影响相比对照组差异有统计学意义,FTC+P-gp对Hep-2细胞活力影响相比对照组差异有统计学意义(P<0.05)。结论:ABCG2可能主要通过影响化疗药物在细胞中的积聚与外排导致细胞耐药。P-gp产生耐药的方式可能有其他途径。P-gp和ABCG2在不同的化疗药物耐药作用中扮演不同的角色。
Objective: To investigate the role of drug resistance genes MDR1 (P-gp) and ABCG2 in drug resistance of Hep-2 cells. Methods: The effects of MDR1 and ABCG2 inhibitors on the accumulation and efflux of anti-tumor drugs in Hep-2 laryngeal carcinoma cell lines were detected by flow cytometry. The effects of MDR1 and ABCG2 inhibitors on the sensitization of Hep-2 laryngeal carcinoma cell lines influences. Results: The FTC of ABCG2 inhibitor was significantly different from that of the control group in Mitoxantrone uptake and efflux assay in Hep-2 cells. There was no significant difference in P-gp between the two groups When the drugs were Mitoxantrone and Cisplatin, there was no significant difference in the viability of Hep-2 cells between the P-gp and ABCG2 antagonists when compared with the control group. When the anti-tumor drug was Doxorubicin, the effects of FTC and P-gp alone The effect of FTC + P-gp on the viability of Hep-2 cells was not statistically different from that of the control group (P <0.05) The effect of P-gp on the viability of Hep-2 cells was statistically different from that of the control group (P <0.05) when the drug was 5-FU, while FTC + P-gp also had little effect on the drug resistance When Paclitaxel was used as antineoplastic agent, the effect of P-gp on Hep-2 cell viability was significantly different from that of control group. The effect of FTC + P-gp on Hep-2 cell viability was statistically different from that of control group Significance (P <0.05). Conclusion: ABCG2 may cause cell resistance mainly by affecting the accumulation and efflux of chemotherapeutic drugs in cells. There are other ways in which P-gp may develop resistance. P-gp and ABCG2 play different roles in different chemotherapeutic drug resistance.