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Inflammation and tissue homeostasis: the NF-κB system in physiology and malignant progression

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Abstract

Disruption of tissue function activates cellular stress which triggers a number of mechanisms that protect the tissue from further damage. These mechanisms involve a number of homeostatic modules, which are regulated at the level of gene expression by the transactivator NF-κB. This transcription factor shifts between activation and repression of discrete, cell-dependent gene expression clusters. Some of its target genes provide feedback to NF-κB itself, thereby strengthening the inflammatory response of the tissue and later terminating inflammation to facilitate restoration of tissue homeostasis. Disruption of key feedback modules for NF-κB in certain cell types facilitates the survival of clones with genomic aberrations, and protects them from being recognized and eliminated by the immune system, to enable thereby carcinogenesis.

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GIL: Reviewed literature, drafted manuscript, reviewed manuscript, proof-edited the manuscript. KH: drafted the manuscript, proof-read the manuscript. SV: edited the manuscript, proof-read the manuscript and gave final permission for publication.

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Correspondence to Spiros Vlahopoulos.

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Lambrou, G.I., Hatziagapiou, K. & Vlahopoulos, S. Inflammation and tissue homeostasis: the NF-κB system in physiology and malignant progression. Mol Biol Rep 47, 4047–4063 (2020). https://doi.org/10.1007/s11033-020-05410-w

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