Aberrant control of NF-κB in cancer permits transcriptional and phenotypic plasticity, to curtail dependence on host tissue: molecular mode

Spiros A. Vlahopoulos


The role of the transcription factor NF-κB in shaping the cancer microenvironment is becoming increasingly clear. Inflammationalters the activity of enzymes that modulate NF-κB function, and causes extensive changes in genomic chromatin that ultimatelydrastically alter cell-specific gene expression. NF-κB regulates the expression of cytokines and adhesion factors that controlinteractions among adjacent cells. As such, NF-κB fine tunes tissue cellular composition, as well as tissues' interactions with theimmune system. Therefore, NF-κB changes the cell response to hormones and to contact with neighboring cells. Activating NF-κBconfers transcriptional and phenotypic plasticity to a cell and thereby enables profound local changes in tissue function andcomposition. Research suggests that the regulation of NF-κB target genes is specifically altered in cancer. Such alterations occurnot only due to mutations of NF-κB regulatory proteins, but also because of changes in the activity of specific proteostatic modulesand metabolic pathways. This article describes the molecular mode of NF-κB regulation with a few characteristic examples oftarget genes.


Cytokine; mucin; chemokine; IL-8/CXCL8; MUC1; NF-κB; IL-6; TNFα

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