Evidence map›Paper›PMID 22695319›Full record

ArticleBMC cancer2012

The role of TGFBI in mesothelioma and breast cancer: association with tumor suppression.

Bingyan Li, Gengyun Wen, Yongliang Zhao, Jian Tong, Tom K Hei

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

34 citing papers in PubMed, 71 citations in OpenAlex.

  1. Trial
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  16. The Clinical Significance ofOncoTargets and therapy · 2020
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  18. Weighted Gene Co-Expression Network Analysis Identifies Hub Genes Associated with Occurrence and Prognosis of Oral Squamous Cell Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2019
    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

5 authors at 2 institutions in 2 countries.

Bingyan LiSchool of Radiation Medicine and Public Health, Soochow University, Suzhou, China.
Gengyun Wen
Yongliang Zhao
Jian Tong
Tom K Hei
Soochow University · CNColumbia University · US

Funding

Training CoreP42ES010349 · NIEHS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI NAVAS-ACIEN, ANA · 2000 to 2020
$53.6M
True Metal fac coreP30ES009089 · NIEHS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MATTHEW S PERZANOWSKI · 1998 to 2026
$44.7M
THE FUNCTIONAL GENOMICS OF BYSTANDER RESPONSESP01CA049062 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI HEI, TOM K. · 1990 to 2014
$21.9M
NCI NIH HHS CA49062NIEHS NIH HHS ES05786NIEHS NIH HHS P30 ES 09089NIEHS NIH HHS P42 ES10349
6 · The paper itself

Abstract

backgroundTransforming growth factor β induced (TGFBI) product, an extracellular matrix (ECM) protein, has been implicated as a putative tumor suppressor in recent studies. Our previous findings revealed that expression of TGFBI gene is down-regulated in a variety of cancer cell lines and clinical tissue samples. In this study, ectopic expression of TGFBI was used to ascertain its role as a tumor suppressor and to determine the underlying mechanism of mesothelioma and breast cancer.

methodsCells were stably transfected with pRc/CMV2-TGFBI and pRc/CMV2-empty vector with Lipofectamine Plus. Ectopic expression of TGFBI was quantified by using quantitative PCR and Western-blotting. Characterization of cell viability was assessed using growth curve, clonogenic survival and soft agar growth. The potential of tumor formation was evaluated by an in vivo mouse model. Cell cycle was analyzed via flow cytometry. Expressions of p21, p53, p16 and p14 were examined using Western-blotting. Senescent cells were sorted by using a Senescence β-Galactosidase Staining Kit. Telomerase activity was measured using quantitative telomerase detection kit.

resultsIn this study, an ectopic expression of TGFBI in two types of cancer cell lines, a mesothelioma cell line NCI-H28 and a breast cancer cell line MDA-MB-231 was found to have reduced the cellular growth, plating efficiency, and anchorage-independent growth. The tumorigenicity of these cancer cell lines as determined by subcutaneous inoculation in nude mice was similarly suppressed by TGFBI expression. Likewise, TGFBI expression reduced the proportion of S-phase while increased the proportion of G1 phase in these cells. The redistribution of cell cycle phase after re-expression of TGFBI was correspondent with transiently elevated expression of p21 and p53. The activities of senescence-associated β-galactosidase and telomerase were enhanced in TGFBI-transfected cells.

conclusionCollectively, these results imply that TGFBI plays a suppressive role in the development of mesothelioma and breast cancer cells, possibly through inhibitions of cell proliferation, delaying of G1-S phase transition, and induction of senescence.

Indexed as

AnimalsBreast NeoplasmsCell CycleCell Line, TumorCell ProliferationCell Transformation, NeoplasticCellular SenescenceFemaleGene ExpressionGene Expression Regulation, NeoplasticHumansMaleMesotheliomaMiceMice, NudeTransforming Growth Factor beta1Transforming Growth Factor beta1

Identifiers

PMID22695319
PMCPMC3480943
OpenAlexW2154149568

What OpenQuestion holds

Textmetadata
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.