Evidence map›Paper›PMID 23691361›Full record

ArticleISRN oncology2013

Endocytic adaptor protein epsin is elevated in prostate cancer and required for cancer progression.

Kandice L Tessneer, Satish Pasula, Xiaofeng Cai, Yunzhou Dong, Xiaolei Liu, Lili Yu, Scott Hahn, John McManus, Yiyuan Chen, Baojun Chang and 1 more

Open access · diamondAbstract read
In one paragraph

Article in ISRN oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Endocytosis in cancer and cancer therapy.Nature reviews. Cancer · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Endocytic Adaptors in Cardiovascular Disease.Frontiers in cell and developmental biology · 2020
    Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Motif mimetic of epsin perturbs tumor growth and metastasis.The Journal of clinical investigation · 2015
    Article
  16. Article
  17. 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

11 authors at 1 institution in 1 country.

Kandice L TessneerCardiovascular Biology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA.
Satish Pasula
Xiaofeng Cai
Yunzhou Dong
Xiaolei Liu
Lili Yu
Scott Hahn
John McManus
Yiyuan Chen
Baojun Chang
Hong Chen
Oklahoma Medical Research Foundation · US

Funding

SWI/SNF-REGULATED POSTNATAL ANGIOGENESISP20RR018758 · NCRR · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI MCEVER, RODGER PAUL · 2003 to 2011
$14.9M
Epsin in Angiogenesis and Vascular RemodelingR01HL093242 · NHLBI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI CHEN, HONG, WANG, DA-ZHI · 2009 to 2021
$7.3M
Molecular Mechanisms Regulating Endothelial DysfunctionR01HL137229 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, SRIVASTAVA, SANJAY · 2017 to 2020
$2.7M
NCRR NIH HHS P20 RR018758NHLBI NIH HHS R01 HL093242NHLBI NIH HHS R01 HL137229
6 · The paper itself

Abstract

Epsins have an important role in mediating clathrin-mediated endocytosis of ubiquitinated cell surface receptors. The potential role for epsins in tumorigenesis and cancer metastasis by regulating intracellular signaling pathways has largely not been explored. Epsins are reportedly upregulated in several types of cancer including human skin, lung, and canine mammary cancers. However, whether their expression is elevated in prostate cancer is unknown. In this study, we investigated the potential role of epsins in prostate tumorigenesis using the wild type or epsin-deficient human prostate cancer cells, LNCaP, in a human xenograft model, and the spontaneous TRAMP mouse model in wild type or epsin-deficient background. Here, we reported that the expression of epsins 1 and 2 is upregulated in both human and mouse prostate cancer cells and cancerous tissues. Consistent with upregulation of epsins in prostate tumors, we discovered that depletion of epsins impaired tumor growth in both the human LNCaP xenograft and the TRAMP mouse prostate. Furthermore, epsin depletion significantly prolonged survival in the TRAMP mouse model. In summary, our findings suggest that epsins may act as oncogenic proteins to promote prostate tumorigenesis and that depletion or inhibition of epsins may provide a novel therapeutic target for future prostate cancer therapies.

Identifiers

PMID23691361
PMCPMC3649151
OpenAlexW2079921447

What OpenQuestion holds

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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.