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10.20892/j.issn.2095-3941.2017.0029

http://scihub22266oqcxt.onion/10.20892/j.issn.2095-3941.2017.0029
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suck abstract from ncbi


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pmid28884042
      Cancer+Biol+Med 2017 ; 14 (3 ): 254-270
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  • Aberrant control of NF-?B in cancer permits transcriptional and phenotypic plasticity, to curtail dependence on host tissue: molecular mode #MMPMID28884042
  • Vlahopoulos SA
  • Cancer Biol Med 2017[Aug]; 14 (3 ): 254-270 PMID28884042 show ga
  • The role of the transcription factor NF-?B in shaping the cancer microenvironment is becoming increasingly clear. Inflammation alters the activity of enzymes that modulate NF-?B function, and causes extensive changes in genomic chromatin that ultimately drastically alter cell-specific gene expression. NF-?B regulates the expression of cytokines and adhesion factors that control interactions among adjacent cells. As such, NF-?B fine tunes tissue cellular composition, as well as tissues' interactions with the immune system. Therefore, NF-?B changes the cell response to hormones and to contact with neighboring cells. Activating NF-?B 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-?B target genes is specifically altered in cancer. Such alterations occur not only due to mutations of NF-?B 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-?B regulation with a few characteristic examples of target genes.
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