Evidence map›Paper›PMID 22496368›Full record

ArticleThe Journal of biological chemistry2012

Signal transducer and activator of transcription 3 (STAT3) protein suppresses adenoma-to-carcinoma transition in Apcmin/+ mice via regulation of Snail-1 (SNAI) protein stability.

Jongdae Lee, Joanna C K Kim, Shee-Eun Lee, Christine Quinley, HyeRi Kim, Scott Herdman, Maripat Corr, Eyal Raz

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.6field-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

48 citing papers in PubMed, 70 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Jongdae LeeDepartment of Medicine, University of California at San Diego, La Jolla, California 92093-0663, USA. j142lee@ucsd.edu
Joanna C K Kim
Shee-Eun Lee
Christine Quinley
HyeRi Kim
Scott Herdman
Maripat Corr
Eyal Raz
University of California, San Diego · US

Funding

TL MOLECULES AND GAMMA-DELTA T CELLSP01DK035108 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KAGNOFF, MARTIN FREDERICK · 1986 to 2013
$19.2M
U of Calif, San Diego Neuroscience Microscopy ImagingP30NS047101 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLEESON, JOSEPH G, ZHENG, BINHAI · 2003 to 2022
$9.0M
The UCSD Digestive Diseases Research Development CenterR24DK080506 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ECKMANN, LARS · 2008 to 2012
$2.7M
The diverse contribution of TLR pathways to intestinal homeostasisR01AI068685 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RAZ, EYAL · 2007 to 2011
$1.9M
Th17 subsets: Differential roles in immune defense mechanisms at the G-I mucosaU01AI095623 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RAZ, EYAL · 2011 to 2015
$1.6M
NIAID NIH HHS AI068685NIAID NIH HHS AI095623NIAID NIH HHS R01 AI068685NIAID NIH HHS U01 AI095623NIDDK NIH HHS DK080506NIDDK NIH HHS DK35108NIDDK NIH HHS P01 DK035108NIDDK NIH HHS R24 DK080506NINDS NIH HHS P30 NS047101
6 · The paper itself

Abstract

STAT3 was recently reported to suppress tumor invasion in Apc(min)(/+) mice. We investigated the mechanisms by which STAT3 inhibits intestinal epithelial tumors using Apc(min)(/+)/Stat3(IEC-KO) mice (intestinal epithelial cell (IEC)-specific deletion of STAT3 in the Apc(min)(/+) background) to determine the role of STAT3 in carcinogenesis in vivo as well as colorectal cancer cell lines in vitro. To inhibit invasion of IEC tumors, STAT3 functions as a molecular adaptor rather than a transcription factor. Accordingly, the tumors in Apc(min)(/+)/Stat3(IEC-KO) mice undergo adenoma-to-carcinoma transition and acquire an invasive phenotype. Similarly, STAT3 knockdown in a colorectal cell line enhances IEC invasion. We demonstrate that STAT3 down-regulates SNAI (Snail-1) expression levels and hence suppresses epithelial-mesenchymal transition of colorectal cancer cells. Mechanistically, STAT3 facilitates glycogen synthase kinase (GSK) 3β-mediated degradation of SNAI by regulating phosphorylation of GSK3β. Our data identified a new role for STAT3 in the adenoma-to-carcinoma sequence of intestinal tumors.

Indexed as

Genes, APCAdenomaAnimalsBase SequenceCarcinomaCell ProliferationDNA PrimersDown-RegulationEpithelial-Mesenchymal TransitionIntestinal NeoplasmsMiceMice, KnockoutPolymerase Chain ReactionRNA, Small InterferingSnail Family Transcription FactorsSTAT3 Transcription FactorDNA PrimersRNA, Small InterferingSnai1 protein, mouseSnail Family Transcription FactorsStat3 protein, mouseSTAT3 Transcription FactorTranscription Factors

Identifiers

PMID22496368
PMCPMC3365759
OpenAlexW2002986373

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.