作者: Gon Sup Kim , Soon Chan Hong , Bae Kwon Jeong , Won Sup Lee , Jin-Myung Jung
DOI: 10.3390/IJMS22094940
关键词: Chemistry 、 Cell 、 Cancer stem cell 、 Programmed cell death 、 Cancer research 、 MAPK/ERK pathway 、 Apoptosis 、 Necroptosis 、 CD44 、 Cancer
摘要: Breast cancer is one of the major causes deaths due to cancer, especially in women. The crucial barrier for breast treatment resistance radiation therapy, important local regional therapies. We previously established and characterized radio-resistant MDA-MB-231 cells (RT-R-MDA-MB-231 cells) that harbor a high expression stem (CSCs) EMT phenotype. In this study, we performed antibody array analysis identify hub signaling mechanism RT-R-MDA-MB-231 by comparing parental (p-MDA-MB-231) cells. Antibody unveiled MAPK1 protein was most upregulated compared p-MDA-MB-231 pathway enrichment also revealed presence almost all enriched pathways. Thus, used an MEK/ERK inhibitor, PD98059, block role radio-resistance inhibition induced cell death both cells, but each different; underwent apoptosis, showing shrinkage PARP-1 cleavage, while necroptosis, mitochondrial dissipation, nuclear swelling, increase expressions CypA AIF. addition, reversed suppressed increased CSC markers (CD44 OCT3/4) phenotype (β-catenin N-cadherin/E-cadherin). Taken together, study suggests activated ERK signals related