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Cited by 1,160Cytokine Signaling Pathways and InteractionsNF-κB Signaling PathwaysSignaling Pathways in Disease

Dangerous liaisons: STAT3 and NF-κB collaboration and crosstalk in cancer

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Grivennikov, Sergei I., Karin, Michael·2010·Cytokine & Growth Factor Reviews
DOI 10.1016/j.cytogfr.2009.11.005PMC PMC2834864
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Abstract

Transcriptional factors of the NF-kappaB family and STAT3 are ubiquitously expressed and control numerous physiological processes including development, differentiation, immunity, metabolism and cancer. Both NF-kappaB and STAT3 are rapidly activated in response to various stimuli including stresses and cytokines, although they are regulated by entirely different signaling mechanisms. Once activated, NF-kappaB and STAT3 control the expression of anti-apoptotic, pro-proliferative and immune response genes. Some of these genes overlap and require transcriptional cooperation between the two factors. The activation of and interaction between STAT3 and NF-kappaB plays a key role in controlling the dialog between the malignant cell and its microenvironment, especially with inflammatory/immune cells that infiltrate tumors. Quite often, cytokines whose expression is induced in response to NF-kappaB in immune cells of the tumor microenvironment lead to STAT3 activation in both malignant and immune cells. While within malignant and pre-malignant cells STAT3 exerts important oncogenic functions, within inflammatory cells it may also suppress tumor promotion through its anti-inflammatory effects. Other interactions and forms of crosstalk between NF-kappaB and STAT3 include physical interaction between the two, cooperation of these factors at gene promoters/enhancers, the NF-kappaB dependent expression of inhibitors of STAT3 activation and the participation of STAT3 in inflammatory cells in the negative regulation NF-kappaB. Despite these versatile and occasionally antagonistic interactions, NF-kappaB and STAT3 cooperate to promote the development and progression of colon, gastric and liver cancers. In addition to explaining the molecular pathogenesis of cancer, these interactions also offer opportunities for the design of new therapeutic interventions.

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  • Either or both STAT3 and NF-κB are activated in a variety of tumors, including lung, breast, pancreatic and prostate cancers.

    “Either or both of STAT3 and NF-κB are activated in a variety of tumors, including lung, breast, pancreatic and prostate cancers (67).”

    From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [67]

    The STAT3 section (page unavailable) reports activated STAT3 in breast, lung and prostate cancers, and the Introduction describes NF-κB and STAT3 activation across malignancies. Our copy does not identify pancreatic cancer among the examples, so that part of the attributed list is unsupported (searched: pancreatic). (LLM, conf=0.85)

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  • NF-κB and STAT3 play crucial roles in cancer development and progression.

    “Furthermore, NF-κB and STAT3 play crucial roles in cancer development and progression (19, 25, 67, 279).”

    From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [67]

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Authors
Grivennikov, S. I., & Karin, M.
Affiliations
University of California San Diego (US)
Corresponding author
Karin, Michael
ORCID
Venue
Cytokine & Growth Factor Reviews
Publisher
Elsevier BV
Published
2010-02
Volume
21
Issue
1
Pages
11-19
ISSN
1359-6101 (ISSN-L)
DOI
10.1016/j.cytogfr.2009.11.005
PMC
PMC2834864
OpenAlex
W2081107312
Cited by
1,160
References
11
Citations by year
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FWCI
4.06
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Cytokine & Growth Factor Reviews (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • American Cancer Society
  • National Institutes of Health
  • National Cancer Institute (R01CA118165)
Topics
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords
STAT3, NF-κB, transcription factor crosstalk, transcriptional cooperation, tumor microenvironment, tumor-infiltrating immune cells, cytokines, anti-inflammatory activity, colon cancer, gastric cancer, liver cancer, oncogenic signaling, therapeutic target
MeSH terms
Animals, Colitis, Colonic Neoplasms, Humans, Models, Biological, Neoplasms, Neovascularization, Pathologic, Oncogenes, Transcription Factors, Signal Transduction, Cell Hypoxia, Gene Expression Regulation, Neoplastic, Cytokines, NF-kappa B, Chemokines, STAT3 Transcription Factor, Mice

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