Volume 2, 2019
Disruption of homeostasis-induced signaling and crosstalk in the carcinogenesis paradigm “Epistemology of the origin of cancer”
|Number of page(s)||35|
|Section||Life Sciences - Medicine|
|Published online||10 May 2019|
NF-κB signaling and crosstalk during carcinogenesis
Theodor-Billroth-Academy ®, Germany, USA
2 INCORE, International Consortium of Research Excellence of the Theodor-Billroth-Academy ®, Germany, USA
3 Department of Surgery, Carl-Thiem-Klinikum, Cottbus, Germany
4 Department of Physiology, University of Tübingen, Tübingen, Germany
5 Risk-Based Decisions Inc., Sacramento, CA, USA
* Corresponding author: email@example.com
Accepted: 9 April 2019
Transcription factors (TFs) are proteins that control the transcription of genetic information from DNA to mRNA by binding to specific DNA sequences either on their own or with other proteins as a complex. TFs thus support or suppress the recruitment of the corresponding RNA polymerase. In general, TFs are classified by structure or function. The TF, Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), is expressed in all cell types and tissues. NF-κB signaling and crosstalk are involved in several steps of carcinogenesis including in sequences involving pathogenic stimulus, chronic inflammation, fibrosis, establishment of its remodeling to the precancerous niche (PCN) and transition of a normal cell to a cancer cell. Triggered by various inflammatory cytokines, NF-κB is activated along with other TFs with subsequent stimulation of cell proliferation and inhibition of apoptosis. The involvement of NF-κB in carcinogenesis provides an opportunity to develop anti-NF-κB therapies. The complexity of these interactions requires that we elucidate those aspects of NF-κB interactions that play a role in carcinogenesis, the sequence of events leading to cancer.
Key words: α-SMA / AFT3 / AMPK / ANXA2 / AP1 / APO-1 / BAG-1 / Barrett / Bcl-2 / BiP / Cancer / Carcinogenesis / CCC / CD54 / CD95 / CD106 / cdk2 / CDX2 / Cell transition / Chronic inflammation / Cox-2 / cRel / CXCL8 / Cyclin B1 / Cyclin D1 / C/EBPβ / EBV / ECM / EGFR / ELAM-1 / Epstein-Barr virus / E-selectin / Fas / Fibrosis / GC-C / GERD / Ghrelin / GHS-R / GM-CSF / GTPase / HBV / HBx / HCC / HCV / Helicobacter / Hepatitis / HIAP / HPV / H-ras / hTERT / ICAM-1 / IκBα / IκBβ / IκBγ / IκBε / IκB kinase (IKK) complex / IKK1 / IKK2 / IKKγ / IL-6 / IL-8 / IL-13 / IL-β1 / iNOS / Lysyl oxidase / LOX / LOXL2 / MAP2K1 / Metallo proteinase / Metaplasia / Microbiome / MIP1α / MMP / MMP-1 / MMP-9 / Morbid obesity / Mycoplasma / M. fermentans / M. hominis / M. penetrans / NEMO / Nuclear factor kappa-light-chain-enhancer of activated B cells / NF-κB / p50 / p52 / p53 / p65 / p100 / Pathogenic stimulus / PLA2 / PRDM1 / RelA / RelB / Remodeling / RHD / Schistosomiasis / S. japonicum / S. mansoni / SOCS2 / STAT3 / TGF-β1 / TF / TLR / TNFα / TRAF1 / TRAF2 / TTF / UPR / VCAM-1 / VEGF
© B.L.D.M. Brücher et al., Published by EDP Sciences, 2019
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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