Evidence map›Paper›PMID 23912451›Full record

ArticleOncogene2014

STAT3 expression, activity and functional consequences of STAT3 inhibition in esophageal squamous cell carcinomas and Barrett's adenocarcinomas.

S Timme, S Ihde, C D Fichter, V Waehle, L Bogatyreva, K Atanasov, I Kohler, A Schöpflin, H Geddert, G Faller and 8 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
4.4field-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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Targeting STAT3 Enzyme for Cancer Treatment.Mini reviews in medicinal chemistry · 2024
    Review
  5. Article
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  11. Review
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  18. [Expression of miR-454-3p and its effect on proliferation, invasion and metastasis of colon cancer].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018
    Article
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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

18 authors at 4 institutions in 2 countries.

S TimmeInstitute of Clinical Pathology, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany.
S IhdeInstitute of Clinical Pathology, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany.
C D Fichter1] Institute of Clinical Pathology, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany [2] Faculty of Biology, Albert-Ludwigs-University, Freiburg, Germany.
V WaehleInstitute of Clinical Pathology, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany.
L BogatyrevaInstitute of Medical Biometry and Medical Informatics, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany.
K AtanasovInstitute of Clinical Pathology, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany.
I KohlerInstitute of Clinical Pathology, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany.
A SchöpflinInstitute of Clinical Pathology, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany.
H GeddertDepartment of Pathology, St Vincentius Kliniken, Karlsruhe, Germany.
G FallerDepartment of Pathology, St Vincentius Kliniken, Karlsruhe, Germany.
D KlimstraDepartment of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
L TangDepartment of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
T Reinheckel1] Institute of Molecular Medicine and Cell Research, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany [2] BIOSS Centre for Biological Signalling Studies, Albert-Ludwigs-University, Freiburg, Germany [3] Comprehensive Cancer Center Freiburg, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany.
D HauschkeInstitute of Medical Biometry and Medical Informatics, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany.
H Busch1] Institute of Molecular Medicine and Cell Research, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany [2] German Cancer Consortium (DKTK), Heidelberg, Germany [3] German Cancer Research Center (DKFZ), Heidelberg, Germany.
M Boerries1] Institute of Molecular Medicine and Cell Research, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany [2] German Cancer Consortium (DKTK), Heidelberg, Germany [3] German Cancer Research Center (DKFZ), Heidelberg, Germany.
M Werner1] Institute of Clinical Pathology, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany [2] Comprehensive Cancer Center Freiburg, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany [3] German Cancer Consortium (DKTK), Heidelberg, Germany [4] German Cancer Research Center (DKFZ), Heidelberg, Germany.
S Lassmann1] Institute of Clinical Pathology, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany [2] BIOSS Centre for Biological Signalling Studies, Albert-Ludwigs-University, Freiburg, Germany [3] Comprehensive Cancer Center Freiburg, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany [4] German Cancer Consortium (DKTK), Heidelberg, Germany [5] German Cancer Research Center (DKFZ), Heidelberg, Germany.
University of Freiburg · DEMemorial Sloan Kettering Cancer Center · USSt. Vincentius-Kliniken · DEUniversity Medical Center Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Signal transducer and activator of transcription 3 (STAT3) is altered in several epithelial cancers and represents a potential therapeutic target. Here, STAT3 expression, activity and cellular functions were examined in two main histotypes of esophageal carcinomas. In situ, immunohistochemistry for STAT3 and STAT3-Tyr705 phosphorylation (P-STAT3) in esophageal squamous cell carcinomas (ESCC, n=49) and Barrett's adenocarcinomas (BAC, n=61) revealed similar STAT3 expression in ESCCs and BACs (P=0.109), but preferentially activated P-STAT3 in ESCCs (P=0.013). In vitro, strong STAT3 activation was seen by epidermal growth factor (EGF) stimulation in OE21 (ESCC) cells, whereas OE33 (BAC) cells showed constitutive weak STAT3 activation. STAT3 knockdown significantly reduced cell proliferation of OE21 (P=0.0148) and OE33 (P=0.0243) cells. Importantly, STAT3 knockdown reduced cell migration of OE33 cells by 2.5-fold in two types of migration assays (P=0.073, P=0.015), but not in OE21 cells (P=0.1079, P=0.386). Investigation of transcriptome analysis of STAT3 knockdown revealed a reduced STAT3 level associated with significant downregulation of cell cycle genes in both OE21 (P<0.0001) and OE33 (P=0.01) cells. In contrast, genes promoting cell migration (CTHRC1) were markedly upregulated in OE21 cells, whereas a gene linked to tight-junction stabilization and restricted cell motility (SHROOM2) was downregulated in OE21 but upregulated in OE33 cells. This study shows frequent, but distinct, patterns of STAT3 expression and activation in ESCCs and BACs. STAT3 knockdown reduces cell proliferation in ESCC and BAC cells, inhibits migration of BAC cells and may support cell migration of ESCC cells. Thereby, novel STAT3-regulated genes involved in ESCC and BAC cell proliferation and cell migration were identified. Thus, STAT3 may be further exploited as a potential novel therapeutic target, however, by careful distinction between the two histotypes of esophageal cancers.

Indexed as

AdenocarcinomaBarrett EsophagusCarcinoma, Squamous CellCell CycleCell Growth ProcessesCell Line, TumorCell MovementDown-RegulationEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaGene Knockdown TechniquesHumansPhosphorylationSignal TransductionSTAT3 Transcription FactorUp-RegulationSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID23912451
OpenAlexW2041198543

What OpenQuestion holds

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Registered trials

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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.