IκBα targeting promotes oxidative stress-dependent cell death.
Giovanna CarràGiuseppe ErmondiChiara RigantiLuisella RighiGiulia CaronAlessio MengaEnrica CapellettoBeatrice MaffeoMarcello Francesco LinguaFederica FusellaMarco VolanteRiccardo TaulliAngelo GuerrasioSilvia NovelloMara BrancaccioRocco PiazzaAlessandro MorottiPublished in: Journal of experimental & clinical cancer research : CR (2021)
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.
Keyphrases
- cell death
- oxidative stress
- cell cycle arrest
- cell proliferation
- papillary thyroid
- transcription factor
- dna damage
- squamous cell
- reactive oxygen species
- ischemia reperfusion injury
- genome wide
- cancer therapy
- nucleic acid
- gene expression
- drug delivery
- childhood cancer
- young adults
- signaling pathway
- endoplasmic reticulum