Evidence map›Paper›PMID 26517089›Full record

ArticleOncotarget2015

Aberrantly upregulated TRAP1 is required for tumorigenesis of breast cancer.

Bo Zhang, Jing Wang, Zhen Huang, Peng Wei, Ying Liu, Junfeng Hao, Lijing Zhao, Fenglin Zhang, Yaping Tu, Taotao Wei

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 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
2.9field-weighted citation impact, top 9% 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, 62 citations in OpenAlex.

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  4. TRAP1 and its therapeutic potential.Bioorganic & medicinal chemistry letters · 2025
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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 2 countries.

Bo ZhangNational Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Jing WangDepartment of Breast Surgical Oncology, Cancer Hospital, Chinese Academy of Medical Sciences, Beijing, China.
Zhen HuangDepartment of Breast Surgical Oncology, Cancer Hospital, Chinese Academy of Medical Sciences, Beijing, China.
Peng WeiNational Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Ying LiuSchool of Basic Medical Sciences, Hubei University of Medicine, Shiyan, Hubei, China.
Junfeng HaoNational Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Lijing ZhaoNational Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Fenglin ZhangNational Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Yaping TuDepartment of Pharmacology, Creighton University School of Medicine, Omaha, Nebraska, USA.
Taotao WeiNational Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Institute of Biophysics · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNChinese Academy of Sciences · CNCreighton University · USHubei University of Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor necrosis factor receptor-associated protein 1 (TRAP1) is abnormally expressed in many cancers. In this study, we showed that TRAP1 is aberrantly upregulated in breast tumors compared to control tissues. TRAP1 knockdown downregulates mitochondrial aerobic respiratory, sensitizes cells to lethal stimuli, and inhibited tumor growth in MDA-MB-231 and MCF-7 breast cancer cells in vivo. TRAP1 overexpression, however, enhances the capacity to cope with stress conditions. These evidences suggested that TRAP1 is required for tumorigenesis. We also found that TRAP1 regulates the mitochondrial morphology. Relatively lower TRAP1 levels are associated with the rod-shaped mitochondrial phenotype in invasive and metastatic MDA-MB-231 breast cancer cells; on the contrary, higher TRAP1 levels are associated with the tubular network-shaped mitochondrial phenotype in non-invasive MCF-7 cells. Interestingly, the expression of TRAP1 in human breast cancer specimens inversely correlates with tumor grade. Overexpression of TRAP1 in MDA-MB-231 cells causes mitochondrial fusion, triggers mitochondria to form tubular networks, and suppresses cell migration and invasion in vitro and in vivo. These data link TRAP1-regulated mitochondrial dynamics and function with tumorigenesis of breast cancer and suggested that TRAP1 may therefore be a potential target for breast cancer drug development.

Indexed as

AgedAnimalsBiomarkers, TumorBreast NeoplasmsCarcinogenesisCell MovementFemaleGene Expression Regulation, NeoplasticHSP90 Heat-Shock ProteinsHumansMCF-7 CellsMice, NudeMiddle AgedMitochondriaMitochondrial DynamicsNeoplasm GradingBiomarkers, TumorHSP90 Heat-Shock ProteinsTRAP1 protein, humanbreast cancermetastasismitochondriaTRAP1tumorigenesis

Identifiers

PMID26517089
PMCPMC4792571
OpenAlexW2158264375

What OpenQuestion holds

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LicenceCC BY
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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.