Evidence map›Paper›PMID 25889002›Full record

ArticleMolecular cancer2015

The role of TGFBI (βig-H3) in gastrointestinal tract tumorigenesis.

Bing Han, Haolei Cai, Ying Chen, Bing Hu, Hongyu Luo, Yulian Wu, Jiangping Wu

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

36 citing papers in PubMed, 51 citations in OpenAlex.

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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 2 institutions in 2 countries.

Bing HanLaboratory of Immunology and Cardiovascular Research, Centre hospitalier de l'Université de Montréal (CRCHUM), 900 Stain-Denis Street, Montreal, Quebec, Canada. icehan76@hotmail.com.
Haolei CaiDepartment of Surgery, The Second Affiliated Hospital of Zhejiang University, 88 Jiefang Road, Hangzhou, China. comethalley@hotmail.com.
Ying ChenDepartment of Surgery, The Second Affiliated Hospital of Zhejiang University, 88 Jiefang Road, Hangzhou, China. chy1983@163.com.
Bing HuAnatomic Pathology, AmeriPath Central Florida, 8150 Chancellor Dr, Orlando, FL, USA. bhu@ameripath.com.
Hongyu LuoLaboratory of Immunology and Cardiovascular Research, Centre hospitalier de l'Université de Montréal (CRCHUM), 900 Stain-Denis Street, Montreal, Quebec, Canada. hongyu.luo@umontreal.ca.
Yulian WuDepartment of Surgery, The Second Affiliated Hospital of Zhejiang University, 88 Jiefang Road, Hangzhou, China. wuyulian@medmail.com.cn.
Jiangping WuLaboratory of Immunology and Cardiovascular Research, Centre hospitalier de l'Université de Montréal (CRCHUM), 900 Stain-Denis Street, Montreal, Quebec, Canada. jianping.wu@umontreal.ca.
Centre Hospitalier de l’Université de Montréal · CASecond Affiliated Hospital of Zhejiang University · CN

Funding

Canadian Institutes of Health Research MOP123389Canadian Institutes of Health Research MOP57697
6 · The paper itself

Abstract

backgroundTGFβ-induced (TGFBI/βig-H3) is a protein inducible by TGFβ1 and secreted by many types of cells. It binds to collagen, forms part of the extracellular matrix (ECM), and interacts with integrins on cell surfaces. In this study, we investigated the role of TGFBI in tumorigenesis and the underlying mechanisms.

methodsPatient serum TGFBI levels were determined by ELISA. TGFBI transgenic and gene knockout mice and TGFBI-overexpressing liver cells were used for mechanistic studies.

resultsWe demonstrated that patients with cholangiocarcinomas, hepatic carcinomas or gastric carcinomas presented significantly elevated serum TGFBI levels, and the excess TGFBI was derived from the tumor masses. TGFBI overexpression in mice resulted in increased incidence of spontaneous tumors and N,N-diethylnitrosamine (DEN)-induced liver tumor nodules, compared to that in wild type (WT) mice, while TGFBI knockout mice were comparable to WT controls in these 2 aspects. TGFBI promoted the survival of Aml-12 liver cells with DNA damage after irradiation, and augmented their post-irradiation proliferation. It activated the FAK/AKT/AKT1S1/PRS6/EIF4EBP pathway, which is known to modulate cell survival and proliferation.

conclusionsOur data suggest that TGFBI functions as a promoter of certain gastrointestinal tract cancers. It provides a survival advantage to cells with DNA damage. Over a long time span, this advantage could translate into increased tumor risks.

Indexed as

AnimalsApoptosisbetaIG-H3 ProteinCarcinogenesisCarcinogensCell ProliferationCell SurvivalDNA DamageExtracellular Matrix ProteinsGastrointestinal NeoplasmsGastrointestinal TractHumansLiver NeoplasmsMice, Inbred C57BLMice, KnockoutPhosphorylationbetaIG-H3 ProteinCarcinogensExtracellular Matrix ProteinsTransforming Growth Factor beta

Identifiers

PMID25889002
PMCPMC4435624
OpenAlexW2112621255

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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.