Evidence map›Paper›PMID 23917221›Full record

ArticleOncogenesis2013

Periostin cooperates with mutant p53 to mediate invasion through the induction of STAT1 signaling in the esophageal tumor microenvironment.

G S Wong, J-S Lee, Y-Y Park, A J Klein-Szanto, T J Waldron, E Cukierman, M Herlyn, P Gimotty, H Nakagawa, A K Rustgi

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.8field-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

32 citing papers in PubMed, 49 citations in OpenAlex.

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  9. Clarithromycin Ameliorates Early Brain Injury After Subarachnoid Hemorrhage via Suppressing Periostin-Related Pathways in Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
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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

10 authors at 5 institutions in 1 country.

G S Wong1] Division of Gastroenterology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA [2] Department of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA [3] Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA, USA.
J-S Lee
Y-Y Park
A J Klein-Szanto
T J Waldron
E Cukierman
M Herlyn
P Gimotty
H Nakagawa
A K Rustgi
University of Pennsylvania · USFox Chase Cancer Center · USThe University of Texas MD Anderson Cancer Center · USCancer Research And Biostatistics · USThe Wistar Institute · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Margaret von Mehren · 1985 to 2026
$138.8M
TRANSGENIC AND CHIMERIC MOUSE COREP30DK050306 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Ken Hashigiwa Cadwell · 1997 to 2026
$32.5M
Transformed Esophageal Epithelial Cells and the Tumor MicroenvironmentP01CA098101 · NCI · UNIVERSITY OF PENNSYLVANIA · PI NAKAGAWA, HIROSHI · 2003 to 2023
$31.7M
Training In Tumor VirologyT32CA115299 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ROBERTSON, ERLE S. · 2006 to 2021
$4.7M
3D-Adhesion Stromagenesis in Cancer PermissivenessR01CA113451 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI CUKIERMAN, EDNA · 2006 to 2016
$2.8M
NCI NIH HHS P01 CA098101NCI NIH HHS P30 CA006927NCI NIH HHS R01 CA113451NCI NIH HHS T32 CA115299NIDDK NIH HHS P30 DK050306
6 · The paper itself

Abstract

Periostin (POSTN), a matricellular protein, has been reported to be important in supporting tumor cell dissemination. However, the molecular mechanisms underlying POSTN function within the tumor microenvironment are poorly understood. In this study, we observe that the inducible knockdown of POSTN decreases esophageal squamous cell carcinoma (ESCC) tumor growth in vivo and demonstrate that POSTN cooperates with a conformational missense p53 mutation to enhance invasion. Pathway analyses reveal that invasive esophageal cells expressing POSTN and p53(R175H) mutation display activation of signal transducer and activator of transcription 1 (STAT1) target genes, suggesting that the induction of STAT1 and STAT1-related genes could foster a permissive microenvironment that facilitates invasion of esophageal epithelial cells into the extracellular matrix. Genetic knockdown of STAT1 in transformed esophageal epithelial cells underscores the importance of STAT1 in promoting invasion. Furthermore, we find that STAT1 is activated in ESCC xenograft tumors, but this activation is attenuated with inducible knockdown of POSTN in ESCC tumors. Overall, these results highlight the novel molecular mechanisms supporting the capacity of POSTN in mediating tumor invasion during ESCC development and have implications of therapeutic strategies targeting the tumor microenvironment.

Identifiers

PMID23917221
PMCPMC3759121
OpenAlexW2012590367

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.