Evidence map›Paper›PMID 25284582›Full record

ArticleOncogene2015

Differential roles of STAT3 in the initiation and growth of lung cancer.

Jingjiao Zhou, Zhaoxia Qu, Shapei Yan, Fan Sun, Jeffrey A Whitsett, Steven D Shapiro, Gutian Xiao

Abstract read
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.4field-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

56 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
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  7. PDLIM2 in Lung Adenocarcinoma Metastasis.bioRxiv : the preprint server for biology · 2025
    Article
  8. PDLIM2 Repression: A Common Mechanism in Viral Lung Infection.bioRxiv : the preprint server for biology · 2025
    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

7 authors at 3 institutions in 1 country.

Jingjiao Zhou *University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA.
Zhaoxia Qu *University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA.
Shapei YanUniversity of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA.
Fan SunUniversity of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA.
Jeffrey A WhitsettDivisions of Neonatology, Perinatal and Pulmonary Biology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio 45229, USA.
Steven D ShapiroUniversity of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA.
Gutian XiaoUniversity of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA.
University of Pittsburgh · USUPMC Hillman Cancer Center · USUniversity of Cincinnati · US

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI JOHN C. BYRD · 1988 to 2026
$158.0M
PDLIM2 as a cancer and chemosensitizing targetR01CA172090 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI XIAO, GUTIAN · 2013 to 2017
$1.6M
Modeling ETP-ALL in mouseR21CA175252 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI XIAO, GUTIAN · 2013 to 2014
$360k
NCI NIH HHS P30 CA047904NCI NIH HHS R01 CA172090NCI NIH HHS R21 CA175252
6 · The paper itself

Abstract

Signal transducer and activator of transcription 3 (STAT3) is linked to multiple cancers, including pulmonary adenocarcinoma. However, the role of STAT3 in lung cancer pathogenesis has not been determined. Using lung epithelial-specific inducible knockout strategies, we demonstrate that STAT3 has contrasting roles in the initiation and growth of both chemically and genetically induced lung cancers. Selective deletion of lung epithelial STAT3 in mice before cancer induction by the smoke carcinogen, urethane, resulted in increased lung tissue damage and inflammation, K-Ras oncogenic mutations and tumorigenesis. Deletion of lung epithelial STAT3 after establishment of lung cancer inhibited cancer cell proliferation. Simultaneous deletion of STAT3 and expression of oncogenic K-Ras in mouse lung elevated pulmonary injury, inflammation and tumorigenesis, but reduced tumor growth. These studies indicate that STAT3 prevents lung cancer initiation by maintaining pulmonary homeostasis under oncogenic stress, whereas it facilitates lung cancer progression by promoting cancer cell growth. These studies also provide a mechanistic basis for targeting STAT3 to lung cancer therapy.

Indexed as

AnimalsCell ProliferationCells, CulturedCell Transformation, NeoplasticGene Expression Regulation, NeoplasticImmunoblottingImmunohistochemistryLungLung NeoplasmsMice, KnockoutMice, TransgenicMutationPneumoniaProto-Oncogene Proteins p21(ras)Reverse Transcriptase Polymerase Chain ReactionSTAT3 Transcription FactorHras protein, mouseProto-Oncogene Proteins p21(ras)STAT3 Transcription FactorUrethane

Identifiers

PMID25284582
PMCPMC4387125
OpenAlexW2063799663

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.