@Article{biocell.2026.080867,
AUTHOR = {José Manuel Pérez de la Lastra, Celia María Curieses Andrés, Elena Bustamante Munguira, Celia Andrés Juan, Eduardo Pérez-Lebeña},
TITLE = {From Antagonism to Coexistence: NRF2/NF-κB Co-Activation in Cancer under Chronic Stress},
JOURNAL = {BIOCELL},
VOLUME = {},
YEAR = {},
NUMBER = {},
PAGES = {{pages}},
URL = {http://www.techscience.com/biocell/online/detail/27185},
ISSN = {1667-5746},
ABSTRACT = {Nuclear Factor Erythroid 2-Related Factor 2 (NRF2) and Nuclear Factor kappa B (NF-κB) are central regulators of redox balance and inflammation, and in healthy tissues, their activities are tightly coordinated. Classical models emphasise an antagonistic relationship in which NRF2-driven antioxidant programmes limit the oxidative cues that sustain NF-κB signalling, while inflammatory cascades can restrain cytoprotective responses when robust host defence is required. Increasing evidence from experimental systems and human tumours indicates that this antagonism is frequently relaxed in cancer. Chronic exposure to reactive oxygen species (ROS), cytokines, hypoxia, and mechanical distortion reconfigures the shared regulatory module formed by these transcription factors, allowing stable co-activation rather than mutual exclusion. In many malignancies, NRF2 and NF-κB become simultaneously active, generating hybrid transcriptional states that integrate antioxidant, inflammatory, metabolic, and survival programmes within the same tumour ecosystem.},
DOI = {10.32604/biocell.2026.080867}
}