Evidence map›Paper›PMID 16984731›Full record

ArticleNeoplasia (New York, N.Y.)2006

Molecular cross-talk between the NFkappaB and STAT3 signaling pathways in head and neck squamous cell carcinoma.

Cristiane H Squarize, Rogerio M Castilho, Virote Sriuranpong, Decio S Pinto, Jorge Silvio Gutkind

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed
4.0field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

105 citing papers in PubMed, 171 citations in OpenAlex.

  1. Trial
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  4. Aging and cancer: current understandings and future perspectives.Signal transduction and targeted therapy · 2026
    Review
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  20. Observational

45 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 3 countries.

Cristiane H SquarizeOral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4340, USA.
Rogerio M Castilho
Virote Sriuranpong
Decio S Pinto
Jorge Silvio Gutkind
National Institute of Dental and Craniofacial Research · USUniversidade de São Paulo · BRChulalongkorn University · TH

Funding

Oral CarcinogenesisZIADE000558 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI GUTKIND, JORGE SILVIO · 2009 to 2015
$11.4M
ORAL CARCINOGENESISZ01DE000558 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI GUTKIND, J · 1992 to 2008
$3.6M
6 · The paper itself

Abstract

The development of head and neck squamous cell carcinoma (HNSCC) involves the accumulation of genetic and epigenetic alterations in tumor-suppressor proteins, together with the persistent activation of growth-promoting signaling pathways. The activation of epidermal growth factor receptor (EGFR) is a frequent event in HNSCC. However, EGFR-independent mechanisms also contribute to the activation of key intracellular signaling routes, including signal transducer and activator of transcription-3 (STAT3), nuclear factor kappaB (NFkappaB), and Akt. Indeed, the autocrine activation of the gp130 cytokine receptor in HNSCC cells by tumor-released cytokines, such as IL-6, can result in the EGFR-independent activation of STAT3. In this study, we explored the nature of the molecular mechanism underlying enhanced IL-6 secretion in HNSCC cells. We found that HNSCC cells display an increased activity of the IL-6 promoter, which is dependent on the presence of an intact NFkappaB site. Furthermore, NFkappaB inhibition downregulated IL-6 gene and protein expression, and decreased the release of multiple cytokines. Interestingly, interfering with NFkappaB function also prevented the autocrine/paracrine activation of STAT3 in HNSCC cells. These findings demonstrate a cross-talk between the NFkappaB and the STAT3 signaling systems, and support the emerging notion that HNSCC results from the aberrant activity of a signaling network.

Indexed as

Gene Expression Regulation, NeoplasticCarcinoma, Squamous CellCell Line, TumorCell NucleusDown-RegulationHead and Neck NeoplasmsHumansI-kappa B KinaseInterleukin-6Models, BiologicalNF-kappa BPromoter Regions, GeneticSignal TransductionSTAT3 Transcription FactorTranscription FactorsI-kappa B KinaseInterleukin-6NF-kappa BSTAT3 Transcription FactorTranscription Factors

Identifiers

PMID16984731
PMCPMC1584297
OpenAlexW1972699527

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.