Evidence map›Paper›PMID 30896449›Full record

ArticleJCI insight2019

Human endotrophin as a driver of malignant tumor growth.

Dawei Bu, Clair Crewe, Christine M Kusminski, Ruth Gordillo, Alexandra L Ghaben, Min Kim, Jiyoung Park, Hui Deng, Wei Xiong, Xiao-Zheng Liu and 8 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
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  7. Review
  8. Acute kidney injury is associated with elevated urinary endotrophin.American journal of physiology. Renal physiology · 2025
    Article
  9. Article
  10. The Role ofCancers · 2025
    Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Update on Adipose Tissue and Cancer.Endocrine reviews · 2023
    Article
  17. Article
  18. Article
  19. Plasma endotrophin, reflecting tissue fibrosis, is associated with graft failure and mortality in KTRs: results from two prospective cohort studies.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023
    Article
  20. The UCMD-CausingHuman mutation · 2023
    Article
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

18 authors at 7 institutions in 4 countries.

Dawei BuTouchstone Diabetes Center, Departments of Internal Medicine and Simmons Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Clair CreweTouchstone Diabetes Center, Departments of Internal Medicine and Simmons Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Christine M KusminskiTouchstone Diabetes Center, Departments of Internal Medicine and Simmons Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Ruth GordilloTouchstone Diabetes Center, Departments of Internal Medicine and Simmons Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Alexandra L GhabenTouchstone Diabetes Center, Departments of Internal Medicine and Simmons Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Min KimDepartment of Biological Sciences, School of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, South Korea.
Jiyoung ParkDepartment of Biological Sciences, School of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, South Korea.
Hui DengTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Wei XiongTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Xiao-Zheng LiuDepartment of Biomedicine, University of Bergen, Bergen, Norway.
Per Eystein LønningDepartment of Clinical Science, Faculty of Medicine, University of Bergen, and Department of Oncology, Haukeland University Hospital, Bergen, Norway.
Nils HalbergDepartment of Biomedicine, University of Bergen, Bergen, Norway.
Adan RiosTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Yujun ChangPanamab, Houston, Texas, USA.
Anneliese GonzalezDivision of Oncology, Department of Internal Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Ningyan ZhangTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Zhiqiang AnTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Philipp E SchererTouchstone Diabetes Center, Departments of Internal Medicine and Simmons Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
The University of Texas Southwestern Medical Center · USBrown Foundation · USUlsan National Institute of Science and Technology · KRUniversity of Bergen · NOHaukeland University Hospital · NOThe University of Texas Health Science Center at Houston · USUniversidad de Panamá · PA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have previously reported that the carboxy-terminal proteolytic cleavage product of the COL6α3 chain that we refer to as "endotrophin" has potent effects on transformed mammary ductal epithelial cells in rodents. Endotrophin (ETP) is abundantly expressed in adipose tissue. It is a chemoattractant for macrophages, exerts effects on endothelial cells and through epithelial-mesenchymal transition (EMT) enhances progression of tumor cells. In a recombinant form, human endotrophin exerts similar effects on human macrophages and endothelial cells as its rodent counterpart. It enhances EMT in human breast cancer cells and upon overexpression in tumor cells, the cells become chemoresistant. Here, we report the identification of endotrophin from human plasma. It is circulating at higher levels in breast cancer patients. We have developed neutralizing monoclonal antibodies against human endotrophin and provide evidence for the effectiveness of these antibodies to curb tumor growth and enhance chemosensitivity in a nude mouse model carrying human tumor cell lesions. Combined, the data validate endotrophin as a viable target for anti-tumor therapy for human breast cancer and opens the possibility for further use of these new reagents for anti-fibrotic approaches in liver, kidney, bone marrow and adipose tissue.

Indexed as

AnimalsAntibodies, Monoclonal, HumanizedAntineoplastic AgentsBiomarkers, TumorBreastBreast NeoplasmsCarcinogenesisCell Line, TumorCollagen Type VIFemaleGene Expression ProfilingHEK293 CellsHumansKaplan-Meier EstimateMiceMice, NudeAntibodies, Monoclonal, HumanizedAntineoplastic AgentsBiomarkers, TumorCOL6A3 protein, humanCollagen Type VIendotrophinPeptide FragmentsAdipose tissueBreast cancerCancerEndocrinologyOncology

Identifiers

PMID30896449
PMCPMC6538351
OpenAlexW2923519438

What OpenQuestion holds

Textmetadata
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.