Dynamic aberrant NF-κB spurs tumorigenesis: A new model encompassing the microenvironment

Επιστημονική δημοσίευση - Άρθρο Περιοδικού uoadl:3002797 20 Αναγνώσεις

Μονάδα:
Ερευνητικό υλικό ΕΚΠΑ
Τίτλος:
Dynamic aberrant NF-κB spurs tumorigenesis: A new model encompassing the microenvironment
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Recently it was discovered that a transient activation of transcription factor NF-κB can give cells properties essential for invasiveness and cancer initiating potential. In contrast, most oncogenes to date were characterized on the basis of mutations or by their constitutive overexpression. Study of NF-κB actually leads to a far more dynamic perspective on cancer: tumors caused by diverse oncogenes apparently evolve into cancer after loss of feedback regulation for NF-κB. This event alters the cellular phenotype and the expression of hormonal mediators, modifying signals between diverse cell types in a tissue. The result is a disruption of stem cell hierarchy in the tissue, and pervasive changes in the microenvironment and immune response to the malignant cells. © 2015 Elsevier Ltd.
Έτος δημοσίευσης:
2015
Συγγραφείς:
Vlahopoulos, S.A.
Cen, O.
Hengen, N.
Agan, J.
Moschovi, M.
Critselis, E.
Adamaki, M.
Bacopoulou, F.
Copland, J.A.
Boldogh, I.
Karin, M.
Chrousos, G.P.
Περιοδικό:
Cytokine and Growth Factor Reviews
Εκδότης:
Elsevier Ireland Ltd
Τόμος:
26
Αριθμός / τεύχος:
4
Σελίδες:
389-403
Λέξεις-κλειδιά:
cyclooxygenase 2; glucocorticoid; hydroxymethylglutaryl coenzyme A reductase inhibitor; immunoglobulin enhancer binding protein; interleukin 1beta; interleukin 23; interleukin 6; proteome; reactive oxygen metabolite; STAT3 protein; transcription factor NANOG; transcription factor RelA; immunoglobulin enhancer binding protein, adaptive immunity; binding site; cancer inhibition; carcinogenesis; cell cycle regulation; cell differentiation; cell function; cell shape; cells by body anatomy; DNA binding; DNA repair; enzyme activity; gene expression; gene product; genome; homeostasis; human; hypercholesterolemia; immune response; inflammation; lymphatic system tumor; mitochondrion; molecular dynamics; nonhuman; oncogene; oncogene myc; oncogene stat3; oxidative stress; phenotype; priority journal; protein expression; protein metabolism; protein phosphorylation; protein protein interaction; Review; signal transduction; stem cell niche; transcription initiation; tumor microenvironment; animal; carcinogenesis; genetics; metabolism; physiology; tumor microenvironment, Animals; Carcinogenesis; Humans; NF-kappa B; Tumor Microenvironment
Επίσημο URL (Εκδότης):
DOI:
10.1016/j.cytogfr.2015.06.001
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