Evidence map›Paper›PMID 26139244›Full record

ArticleCancer research2015

AIP1 Expression in Tumor Niche Suppresses Tumor Progression and Metastasis.

Weidong Ji, Yonghao Li, Yun He, Mingzhu Yin, Huanjiao Jenny Zhou, Titus J Boggon, Haifeng Zhang, Wang Min

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 18 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

8 authors at 1 institution in 1 country.

Weidong JiThe First Affiliated Hospital, Center for Translational Medicine, Sun Yat-sen University, Guangzhou, China.
Yonghao LiState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.
Yun HeSchool of Public Health, Sun Yat-sen University, Guangzhou, China.
Mingzhu YinDepartment of Pathology, Vascular Biology Program/Yale Cancer Center, Yale University School of Medicine, New Haven, Connecticut.
Huanjiao Jenny ZhouDepartment of Pathology, Vascular Biology Program/Yale Cancer Center, Yale University School of Medicine, New Haven, Connecticut.
Titus J BoggonDepartment of Pharmacology, Yale University School of Medicine, New Haven, Connecticut.
Haifeng ZhangDepartment of Pathology, Vascular Biology Program/Yale Cancer Center, Yale University School of Medicine, New Haven, Connecticut.
Wang MinThe First Affiliated Hospital, Center for Translational Medicine, Sun Yat-sen University, Guangzhou, China. Department of Pathology, Vascular Biology Program/Yale Cancer Center, Yale University School of Medicine, New Haven, Connecticut. wang.min@yale.edu.
Sun Yat-sen University · CN

Funding

The role of signaling molecule AIP1 in pathological angiogenesisR01HL115148 · NHLBI · YALE UNIVERSITY · PI KYRIAKIDES, THEMIS R · 2013 to 2021
$3.6M
STRESS SIGNALING PATHWAYS LINKING ENDOTHELIAL INJURY TO GRAFT ARTERIOSCLEROSISR01HL109420 · NHLBI · YALE UNIVERSITY · PI POBER, JORDAN S · 2012 to 2020
$3.3M
NHLBI NIH HHS HL109420NHLBI NIH HHS HL115148NHLBI NIH HHS R01 HL109420NHLBI NIH HHS R01 HL115148
6 · The paper itself

Abstract

Studies from tumor cells suggest that tumor-suppressor AIP1 inhibits epithelial-mesenchymal transition (EMT). However, the role of AIP1 in the tumor microenvironment has not been examined. We show that a global or vascular endothelial cell (EC)-specific deletion of the AIP1 gene in mice augments tumor growth and metastasis in melanoma and breast cancer models. AIP1-deficient vascular environment not only enhances tumor neovascularization and increases premetastatic niche formation, but also secretes tumor EMT-promoting factors. These effects from AIP1 loss are associated with increased VEGFR2 signaling in the vascular EC and could be abrogated by systemic administration of VEGFR2 kinase inhibitors. Mechanistically, AIP1 blocks VEGFR2-dependent signaling by directly binding to the phosphotyrosine residues within the activation loop of VEGFR2. Our data reveal that AIP1, by inhibiting VEGFR2-dependent signaling in tumor niche, suppresses tumor EMT switch, tumor angiogenesis, and tumor premetastatic niche formation to limit tumor growth and metastasis.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBreast NeoplasmsCarrier ProteinsCell Line, TumorEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGuanylate KinasesHumansMelanoma, ExperimentalMiceNeoplasm MetastasisNeovascularization, PathologicProtein Kinase InhibitorsSignal TransductionTumor MicroenvironmentAdaptor Proteins, Signal TransducingCarrier ProteinsGuanylate KinasesKDR protein, humanMAGI2 protein, humanProtein Kinase InhibitorsVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID26139244
PMCPMC4558200
OpenAlexW1909982415

What OpenQuestion holds

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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.