Journal Article Review Epublish 6 citations
PubMed: 37000324 DOI: 10.1007/s12672-023-00644-z
NRF2 and STAT3: friends or foes in carcinogenesis?
Discov Oncol 14(1):37
Authors: Andrea Arena, Maria Anele Romeo, Rossella Benedetti, Maria Saveria Gilardini Montani, Roberta Santarelli, Roberta Gonnella, Gabriella D'Orazi, Mara Cirone
Affiliations
- Department of Experimental Medicine, Sapienza University of Rome, Viale Regina Elena 324, 00161, Rome, Italy.
- Department of Neurosciences, Imaging and Clinical Sciences, University "G. D'Annunzio", 66013, Chieti, Italy.
- School of Medicine, UniCamillus International University, 00131, Rome, Italy.
- Department of Experimental Medicine, Sapienza University of Rome, Viale Regina Elena 324, 00161, Rome, Italy.
Abstract
NRF2 is a transcription factor that plays a pivotal role in carcinogenesis, also through the interaction with several pro-survival pathways. NRF2 controls the transcription of detoxification enzymes and a variety of other molecules impinging in several key biological processes. This perspective will focus on the complex interplay of NRF2 with STAT3, another transcription factor often aberrantly activated in cancer and driving tumorigenesis as well as immune suppression. Both NRF2 and STAT3 can be regulated by ER stress/UPR activation and their cross-talk influences and is influenced by autophagy and cytokines, contributing to shape the microenvironment, and both control the execution of DDR, also by regulating the expression of HSPs. Given the importance of these transcription factors, more investigations aimed at better elucidating the outcome of their networking could help to discover new and more efficacious strategies to fight cancer.
MeSH
Transcription Factors, Carcinogenesis, Neoplasms