Evidence map›Paper›PMID 25356755›Full record

ArticleOncotarget2014

CD151-α3β1 integrin complexes suppress ovarian tumor growth by repressing slug-mediated EMT and canonical Wnt signaling.

Lauren A Baldwin, John T Hoff, Jason Lefringhouse, Michael Zhang, Changhe Jia, Zeyi Liu, Sonia Erfani, Hongyan Jin, Mei Xu, Qing-Bai She and 13 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 46 citations in OpenAlex.

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  15. Integrin-associated CD151 is a suppressor of prostate cancer progression.American journal of translational research · 2020
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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

23 authors at 5 institutions in 1 country.

Lauren A BaldwinDepartment of Pharmacology and Nutritional Science, Department of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY. Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, Department of Pathology & Laboratory Medicine, University of Kentucky, College of Medicine, and Markey Cancer Center, University of Kentucky, Lexington, KY.
John T HoffDepartment of Pharmacology and Nutritional Science, Department of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY. Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, Department of Pathology & Laboratory Medicine, University of Kentucky, College of Medicine, and Markey Cancer Center, University of Kentucky, Lexington, KY.
Jason LefringhouseDepartment of Pharmacology and Nutritional Science, Department of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY. Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, Department of Pathology & Laboratory Medicine, University of Kentucky, College of Medicine, and Markey Cancer Center, University of Kentucky, Lexington, KY.
Michael ZhangDepartment of Pharmacology and Nutritional Science, Department of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY.
Changhe JiaDepartment of Pharmacology and Nutritional Science, Department of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY.
Zeyi LiuDepartment of Pharmacology and Nutritional Science, Department of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY.
Sonia ErfaniDepartment of Pharmacology and Nutritional Science, Department of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY.
Hongyan JinDepartment of Pharmacology and Nutritional Science, Department of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY.
Mei XuDepartment of Pharmacology and Nutritional Science, Department of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY.
Qing-Bai SheDepartment of Pharmacology and Nutritional Science, Department of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY.
John R van NagellDivision of Gynecologic Oncology, Department of Obstetrics and Gynecology, Department of Pathology & Laboratory Medicine, University of Kentucky, College of Medicine, and Markey Cancer Center, University of Kentucky, Lexington, KY.
Chi WangDepartment of Pharmacology and Nutritional Science, Department of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY.
Li ChenDepartment of Pharmacology and Nutritional Science, Department of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY.
Rina PlattnerDepartment of Pharmacology and Nutritional Science, Department of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY.
David M KaetzelDepartment of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland.
Jia LuoDepartment of Pharmacology and Nutritional Science, Department of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY.
Michael LuDepartment of Biomedical Science, Florida Atlantic University, Boca Raton, Florida, United States of America.
Dava WestDivision of Gynecologic Oncology, Department of Obstetrics and Gynecology, Department of Pathology & Laboratory Medicine, University of Kentucky, College of Medicine, and Markey Cancer Center, University of Kentucky, Lexington, KY.
Chunming LiuDepartment of Pharmacology and Nutritional Science, Department of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY.
Fred R UelandDivision of Gynecologic Oncology, Department of Obstetrics and Gynecology, Department of Pathology & Laboratory Medicine, University of Kentucky, College of Medicine, and Markey Cancer Center, University of Kentucky, Lexington, KY.
Ronny DrapkinDepartment of Cancer Biology and Pathology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA.
Binhua P ZhouDepartment of Pharmacology and Nutritional Science, Department of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY.
Xiuwei H YangDepartment of Pharmacology and Nutritional Science, Department of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY.
Markey Cancer Center · USUniversity of Kentucky · USDana-Farber Cancer Institute · USFlorida Atlantic University · USUniversity of Maryland, Baltimore · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI Bernard Mark Evers · 2013 to 2026
$38.3M
ALCOHOL AND BREAST CANCERR01AA017226 · NIAAA · WEST VIRGINIA UNIVERSITY · PI LUO, JIA · 2008 to 2024
$5.2M
Suppression of Melanoma Initiation and Progression by NM23-H1R01CA159871 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI KAETZEL, DAVID M · 2012 to 2016
$2.2M
NCI NIH HHS P30 CA177558NCI NIH HHS R01 CA159871NIAAA NIH HHS R01 AA017226
6 · The paper itself

Abstract

Human ovarian cancer is diagnosed in the late, metastatic stages but the underlying mechanisms remain poorly understood. We report a surprising functional link between CD151-α3β1 integrin complexes and the malignancy of serous-type ovarian cancer. Analyses of clinical specimens indicate that CD151 expression is significantly reduced or diminished in 90% of metastatic lesions, while it remains detectable in 58% of primary tumors. These observations suggest a putative tumor-suppressing role of CD151 in ovarian cancer. Indeed, our analyses show that knocking down CD151 or α3 integrin enhances tumor cell proliferation, growth and ascites production in nude mice. These changes are accompanied by impaired cell-cell contacts and aberrant expression of E-cadherin, Mucin 5AC and fibronectin, largely reminiscent of an epithelial to mesenchymal transition (EMT)-like change. Importantly, Slug, a master regulator of EMT, is markedly elevated. Knocking down Slug partially restores CD151-α3β1 integrin complex-dependent suppression of cell proliferation. Moreover, disruption of these adhesion protein complexes is accompanied by a concomitant activation of canonical Wnt signaling, including elevated levels of β-catenin and Axin-2 as well as resistance to the inhibition in β-catenin-dependent transcriptional complexes. Together, our study demonstrates that CD151-α3β1 integrin complexes regulate ovarian tumor growth by repressing Slug-mediated EMT and Wnt signaling.

Indexed as

AnimalsCell Line, TumorCell ProliferationCystadenocarcinoma, SerousEpithelial-Mesenchymal TransitionFemaleFlow CytometryFluorescent Antibody TechniqueHeterograftsHumansIntegrin alpha3beta1MiceMice, NudeOvarian NeoplasmsSignal TransductionSnail Family Transcription FactorsCD151 protein, humanIntegrin alpha3beta1SNAI1 protein, humanSnai2 protein, mouseSnail Family Transcription FactorsTetraspanin 24Transcription Factors

Identifiers

PMID25356755
PMCPMC4322965
OpenAlexW2129485273

What OpenQuestion holds

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LicenceCC BY
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.