p62/SQSTM1 as an oncotarget mediates cisplatin resistance through activating RIP1‐NF‐κB pathway in human ovarian cancer cells

• DOI: 10.1111/cas.13276
• Publication Date: 2017-05-12T15:52:45Z
• Authors: Xiao‐Yu Yan; Yu Zhang; Juan‐Juan Zhang; Li‐Chao Zhang; Ya‐Nan Liu; Yao Wu; Ya‐Nan Xue; Sheng‐Yao Lu; Jing Su; Lian‐Kun Sun
• Keywords: Ovarian Neoplasms; 0301 basic medicine; Microscopy, Confocal; Blotting, Western; NF-kappa B; Fluorescent Antibody Technique; RNA-Binding Proteins; Antineoplastic Agents; Original Articles; Carcinoma, Ovarian Epithelial; Flow Cytometry; Real-Time Polymerase Chain Reaction; 3. Good health; Nuclear Pore Complex Proteins; 03 medical and health sciences; Drug Resistance, Neoplasm; Cell Line, Tumor; Sequestosome-1 Protein; Humans; Immunoprecipitation; Female; Neoplasms, Glandular and Epithelial; Cisplatin; Signal Transduction

Platinum‐based therapeutic strategies have been widely used in ovarian cancer treatment. However, drug resistance has greatly limited efficacy. Recently, tolerance to cisplatin attributed other factors unrelated DNA . p62 (also known as SQSTM 1) functions a multifunctional hub participating tumorigenesis and may be target. Our previous study showed that was overexpressed drug‐resistant epithelial carcinoma its inhibition increased the sensitivity cisplatin. In this study, we demonstrate activity of NF ‐κB signaling pathway K63‐linked ubiquitination RIP 1 higher cisplatin‐resistant ( SKOV 3/ DDP ) cells compared with parental cells. addition, could reversed by inhibiting expression using si RNA Furthermore, deletion ZZ domain interacts 3 markedly decreased inhibited activation pathway. Moreover, loss from led poor proliferative capacity high levels apoptosis made them more sensitive Collectively, provide evidence is implicated partly dependent on 1. promotes cell proliferation inhibits thus mediating