PT  - JOURNAL ARTICLE
AU  - Vlahopoulos, Spiros A.
TI  - Aberrant control of NF-κB in cancer permits transcriptional and phenotypic plasticity, to curtail dependence on host tissue: molecular mode
AID  - 10.20892/j.issn.2095-3941.2017.0029
DP  - 2017 Aug 01
TA  - Cancer Biology and Medicine
PG  - 254--270
VI  - 14
IP  - 3
4099  - http://www.cancerbiomed.org/content/14/3/254.short
4100  - http://www.cancerbiomed.org/content/14/3/254.full
SO  - Cancer Biol Med2017 Aug 01; 14
AB  - The role of the transcription factor NF-κB in shaping the cancer microenvironment is becoming increasingly clear. Inflammation alters the activity of enzymes that modulate NF-κB function, and causes extensive changes in genomic chromatin that ultimately drastically alter cell-specific gene expression. NF-κB regulates the expression of cytokines and adhesion factors that control interactions among adjacent cells. As such, NF-κB fine tunes tissue cellular composition, as well as tissues' interactions with the immune system. Therefore, NF-κB changes the cell response to hormones and to contact with neighboring cells. Activating NF-κB confers transcriptional and phenotypic plasticity to a cell and thereby enables profound local changes in tissue function and composition. Research suggests that the regulation of NF-κB target genes is specifically altered in cancer. Such alterations occur not only due to mutations of NF-κB regulatory proteins, but also because of changes in the activity of specific proteostatic modules and metabolic pathways. This article describes the molecular mode of NF-κB regulation with a few characteristic examples of target genes.