Doxorubicin induces expression of multidrug resistance-associated protein 1 in human small cell lung cancer cell lines by the c-jun N-terminal kinase pathway
作者： Chie Shinoda , Muneharu Maruyama , Takashi Fujishita , Junichi Dohkan , Hirofumi Oda
DOI: 10.1002/IJC.21094
关键词: Multidrug Resistance-Associated Protein 1 、 Doxorubicin 、 Kinase 、 Biology 、 Immunology 、 Transfection 、 Cancer research 、 Multiple drug resistance 、 c-jun 、 Cell culture 、 Lung cancer 、 Oncology
摘要: Multidrug resistance (MDR) is a major impediment to successful chemotherapy for lung cancer. Overexpression of multidrug resistance-associated protein 1 (MRP1) appears be involved in MDR development cancer cells. A number chemotherapeutic agents including doxorubicin (DOX) were reported induce MRP1 expression human In our study, we investigated the mechanism by which DOX induces small cell (SCLC) lines, GLC4 and NCI-H82. These cells expressed at low levels sensitive DOX. Doxorubicin 50 nM induced marked increase 24 hr, stimulated c-jun N-terminal kinase (JNK) activity. Treatment with JNK inhibitor, SP600125, significantly inhibited induction. Furthermore, transfection JNK1 JNK2 antisense oligonucleotides markedly DOX-induced expression. Chromatin immunoprecipitation assays revealed an enhanced recruitment phosphorylated promoter containing AP-1 site upon stimulation, was pretreatment SP600125. Surprisingly, exposed hr maintained increased least 3 weeks. Pretreatment SP600125 before stimulation blocked appearance phenotype as well induction findings suggest that activation may play essential role SCLC combined treatment inhibitor anticancer drugs prevent abrogation
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