阿霉素通过Stat3-cMyc途径诱导三阴性乳腺癌MDA-MB-468细胞耐药性
DOI: 10.3971/j.issn.1000-8578.2018.18.0497
Keywords: 三阴性乳腺癌,阿霉素,耐药性,Stat3,cMyc,ABCG2,Mechanism of miRNA-451 Regulating Resistance of Gastric Cancer Cells to 5-Fu Through MRP,Tanshinone ⅡA Enhances Chemosensitivity of Breast Cancer Cells to Doxorubicin and Related Mechanism,Feedback Activation of STAT3 Confers Resistance of HER2-positive Breast Cancer Cells to Lapatinib,Silence of STAT3 Enhances SNX-2112-induced Apoptosis of Esophageal Cancer Stem Cells,Expression of Circular RNA ciRS-7 and Its Effect on Invasion and Migration of Triplenegative reast Cancer Cells,Afatinib Sensibilizes Multidrug-resistant Human Ovarian Cancer Cells to Adriamycin and Related Mechanisms,Effect of Two Administration Methods of Endostar Combined with Epirubicin on Breast Cancer in Mice,Reversal Effect of Apatinib on P-gp-mediated Multidrug Resistance of Human Breast Cancer and Its Mechanisms,Analysis E-cad and VEGF Expression in Triple-negative Breast Cancer of Han and Uygur,Knockdown of PKD1 Decreased Sensitivity of Human Salivary Gland Adenoid Cystic Carcinoma Cell Line ACC2 to Paclitaxel,miR-143/145 Cluster Regulate Multi-drug Resistance of Small Cell Lung Cancer,Pharmacodynamics of Doxorubicin Long-circulating Thermo-sensitive Liposomes Combined with Radiofrequency Thermotherapy,Correlation Between Epithelial-mesenchymal Transition and Sensitivity to EGFR Targeted Monoclonal Antibody in Triple Negative Breast Cancer Cells,Establishment of DDP Resistant Variant of Triple Negative Breast Cancer Cell Line MDA-MB-231/DDP and Its Appraisal,Valuation of SUVmax, Ki-67, p53 and EGFR in Predicting Effect of Neoadjuvant Chemotherapy on Triple-negative Breast Cancer Patients
Abstract:
摘要 目的 观察阿霉素(Adriamycin，ADM)对人三阴性乳腺癌MDA-MB-468细胞耐药性的诱导作用并探讨其机制。方法 培养人三阴性乳腺癌MDA-MB-468细胞，用不同浓度阿霉素处理细胞24 h后，MTT法检测细胞生长抑制率及细胞对阿霉素的敏感度。免疫荧光染色法检测耐药蛋白ABCG2的表达；免疫印迹法检测Stat3、p-Stat3、转录因子cMyc及耐药蛋白ABCG2的表达水平。结果 阿霉素持续刺激4周后，获得的MDA-MB-468/ADM细胞对阿霉素的敏感度明显降低，且耐药蛋白ABCG2的表达明显增加；MDA-MB-468/ADM细胞p-Stat3、cMyc及ABCG2的表达量显著增加；MDAMB-468/ADM细胞培养液中加入WP1066后Stat3磷酸化明显抑制，cMyc及ABCG2的表达水平下调，并且MDA-MB-468/ADM细胞对阿霉素的敏感度明显增强（P<0.05）。结论 阿霉素可以通过Stat3-cMyc途径诱导三阴性乳腺癌MDA-MB-468细胞产生耐药性
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