RNF25-Mediated NF-?B Activation Drives Anti-Apoptosis and Therapy Resistance in Cancer
Dysregulation of the NF-?B pathway is frequently observed in cancers, contributing to therapy resistance by inhibiting apoptosis. In this study, we identify RNF25, an E3 ubiquitin ligase, as a key regulator of signal transduction, inflammation, immune responses, and apoptosis. RNA sequencing (RNA-seq) analysis following RNF25 knockdown revealed significant alterations in key apoptotic regulators and NF-?B signaling components, highlighting the role of RNF25 in apoptotic resistance and therapeutic response. Pathway enrichment analysis further demonstrated disruptions in pro-survival and inflammatory signaling pathways, suggesting that RNF25 knockdown enhances apoptotic sensitivity and may influence treatment efficacy. This dataset provides valuable insights into potential therapeutic targets for overcoming treatment resistance. Overall design: To investigate the function of RNF25 in the RCC cell lines in which RNF25 has been knocked down by shRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of control and KD cells with Biological triplicates.