Evidence map›Paper›PMID 26552408›Full record

ArticleEndocrine-related cancer2016

Inhibition of STAT3 activity delays obesity-induced thyroid carcinogenesis in a mouse model.

Jeong Won Park, Cho Rong Han, Li Zhao, Mark C Willingham, Sheue-yann Cheng

Open access · bronzeAbstract read
In one paragraph

Article in Endocrine-related cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.9field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 46 citations in OpenAlex.

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  19. Leptin-induced signaling pathways in cancer cell migration and invasion.Cellular oncology (Dordrecht, Netherlands) · 2019
    Review
  20. Coding Molecular Determinants of Thyroid Cancer Development and Progression.Endocrinology and metabolism clinics of North America · 2019
    Review
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 2 institutions in 1 country.

Jeong Won ParkLaboratory of Molecular BiologyCenter for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Dr, Room 5128, Bethesda, Maryland 20892-6264, USA.
Cho Rong HanLaboratory of Molecular BiologyCenter for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Dr, Room 5128, Bethesda, Maryland 20892-6264, USA.
Li ZhaoLaboratory of Molecular BiologyCenter for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Dr, Room 5128, Bethesda, Maryland 20892-6264, USA.
Mark C WillinghamLaboratory of Molecular BiologyCenter for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Dr, Room 5128, Bethesda, Maryland 20892-6264, USA.
Sheue-yann ChengLaboratory of Molecular BiologyCenter for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Dr, Room 5128, Bethesda, Maryland 20892-6264, USA chengs@mail.nih.gov.
Center for Cancer Research · USNational Institutes of Health · US

Funding

Preclinical Mouse Models of Thyroid CancerZIABC011191 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI CHENG, SHEUE-YANN · 2009 to 2025
$13.8M
Intramural NIH HHS ZIA BC011191
6 · The paper itself

Abstract

Compelling epidemiologic studies indicate that obesity is a risk factor for many human cancers, including thyroid cancer. In recent decades, the incidence of thyroid cancer has dramatically increased along with a marked rise in obesity prevalence. We previously demonstrated that a high fat diet (HFD) effectively induced the obese phenotype in a mouse model of thyroid cancer (Thrb(PV/PV)Pten(+/-) mice). Moreover, HFD activates the STAT3 signal pathway to promote more aggressive tumor phenotypes. The aim of the present study was to evaluate the effect of S3I-201, a specific inhibitor of STAT3 activity, on HFD-induced aggressive cancer progression in the mouse model of thyroid cancer. WT and Thrb(PV/PV)Pten(+/-) mice were treated with HFD together with S3I-201 or vehicle-only as controls. We assessed the effects of S3I-201 on HFD-induced thyroid cancer progression, the leptin-JAK2-STAT3 signaling pathway, and key regulators of epithelial-mesenchymal transition (EMT). S3I-201 effectively inhibited HFD-induced aberrant activation of STAT3 and its downstream targets to markedly inhibit thyroid tumor growth and to prolong survival. Decreased protein levels of cyclins D1 and B1, cyclin dependent kinase 4 (CDK4), CDK6, and phosphorylated retinoblastoma protein led to the inhibition of tumor cell proliferation in S3I-201-treated Thrb(PV/PV)Pten(+/-) mice. Reduced occurrence of vascular invasion and blocking of anaplasia and lung metastasis in thyroid tumors of S3I-201-treated Thrb(PV/PV)Pten(+/-) mice were mediated via decreased expression of vimentin and matrix metalloproteinases, two key effectors of EMT. The present findings suggest that inhibition of the STAT3 activity would be a novel treatment strategy for obesity-induced thyroid cancer.

Indexed as

Aminosalicylic AcidsAnimalsBenzenesulfonatesCarcinogenesisCell ProliferationDiet, High-FatDisease Models, AnimalDown-RegulationEpithelial-Mesenchymal TransitionMiceMice, TransgenicObesityPTEN PhosphohydrolaseSTAT3 Transcription FactorThyroid GlandThyroid Hormone Receptors betaAminosalicylic AcidsBenzenesulfonatesNSC 74859PTEN PhosphohydrolasePten protein, mouseStat3 protein, mouseSTAT3 Transcription FactorThyroid Hormone Receptors betaJAK2-STAT3 signalingobesitypreclinical mouse modelPten-deficiencySTAT3 inhibitorthyroid cancerthyroid hormone receptor β mutant

Identifiers

PMID26552408
PMCPMC4671368
OpenAlexW2178262933

What OpenQuestion holds

Textmetadata
LicenceTDM
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.