I κBα targeting promotes oxidative stress-dependent cell death

CONCLUSIONS: NFKBIA amplification and IκBα overexpression identify a unique cancer subtype associated with specific expression profile and metabolic signatures. Through p65-NFKB regulation, IκBα overexpression favors metabolic rewiring of cancer cells and distinct susceptibility to cisplatin. Lastly, we have developed a novel approach to disrupt IκBα/p65 interaction, restoring p65-mediated apoptotic responses to cisplatin due to mitochondria deregulation and ROS-production.PMID:33863364 | DOI:10.1186/s13046-021-01921-x

Source: Clinical Lung Cancer - April 17, 2021 Category: Cancer & Oncology Authors: Giovanna Carr à Giuseppe Ermondi Chiara Riganti Luisella Righi Giulia Caron Alessio Menga Enrica Capelletto Beatrice Maffeo Marcello Francesco Lingua Federica Fusella Marco Volante Riccardo Taulli Angelo Guerrasio Silvia Novello Mara Brancaccio Rocco Pia Source Type: research