Evidence map›Paper›PMID 25083990›Full record

ArticleThe Journal of clinical investigation2014

Ion channel TRPV1-dependent activation of PTP1B suppresses EGFR-associated intestinal tumorigenesis.

Petrus R de Jong, Naoki Takahashi, Alexandra R Harris, Jihyung Lee, Samuel Bertin, James Jeffries, Michael Jung, Jen Duong, Amy I Triano, Jongdae Lee and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

  1. The Impact of TRPV1 on Cancer Pathogenesis and Therapy: A Systematic Review.International journal of biological sciences · 2021
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Metal Ion Signaling in Biomedicine.Chemical reviews · 2025
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Observational
  15. Article
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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

20 authors at 4 institutions in 4 countries.

Petrus R de Jong
Naoki Takahashi
Alexandra R Harris
Jihyung Lee
Samuel Bertin
James Jeffries
Michael Jung
Jen Duong
Amy I Triano
Jongdae Lee
Yaron Niv
David S Herdman
Koji Taniguchi
Chang-Whan Kim
Hui Dong
Lars Eckmann
Stephanie M Stanford
Nunzio Bottini
Maripat Corr
Eyal Raz
University of California, San Diego · USLa Jolla Institute for Immunology · USNiigata University · JPUniversity Medical Center Utrecht · NL

Funding

TL MOLECULES AND GAMMA-DELTA T CELLSP01DK035108 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KAGNOFF, MARTIN FREDERICK · 1986 to 2013
$19.2M
U of Calif, San Diego Neuroscience Microscopy ImagingP30NS047101 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLEESON, JOSEPH G, ZHENG, BINHAI · 2003 to 2022
$9.0M
Th17 subsets: Differential roles in immune defense mechanisms at the G-I mucosaU01AI095623 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RAZ, EYAL · 2011 to 2015
$1.6M
NIAID NIH HHS AI095623NIAID NIH HHS U01 AI095623NIDDK NIH HHS DK35108NIDDK NIH HHS P01 DK035108NINDS NIH HHS P30 NS047101
6 · The paper itself

Abstract

The intestinal epithelium has a high rate of turnover, and dysregulation of pathways that regulate regeneration can lead to tumor development; however, the negative regulators of oncogenic events in the intestinal epithelium are not fully understood. Here we identified a feedback loop between the epidermal growth factor receptor (EGFR), a known mediator of proliferation, and the transient receptor potential cation channel, subfamily V, member 1 (TRPV1), in intestinal epithelial cells (IECs). We found that TRPV1 was expressed by IECs and was intrinsically activated upon EGFR stimulation. Subsequently, TRPV1 activation inhibited EGFR-induced epithelial cell proliferation via activation of Ca2+/calpain and resulting activation of protein tyrosine phosphatase 1B (PTP1B). In a murine model of multiple intestinal neoplasia (Apc(Min/+) mice), TRPV1 deficiency increased adenoma formation, and treatment of these animals with an EGFR kinase inhibitor reversed protumorigenic phenotypes, supporting a functional association between TRPV1 and EGFR signaling in IECs. Administration of a TRPV1 agonist suppressed intestinal tumorigenesis in Apc(Min/+) mice, similar to--as well as in conjunction with--a cyclooxygenase-2 (COX-2) inhibitor, which suggests that targeting both TRPV1 and COX-2 has potential as a therapeutic approach for tumor prevention. Our findings implicate TRPV1 as a regulator of growth factor signaling in the intestinal epithelium through activation of PTP1B and subsequent suppression of intestinal tumorigenesis.

Indexed as

AnimalsCalciumCalcium ChannelsCalpainCell ProliferationCyclooxygenase 2 InhibitorsEnzyme ActivationErbB ReceptorsHumansIntestinal NeoplasmsMiceProtein Tyrosine Phosphatase, Non-Receptor Type 1Signal TransductionTRPV Cation ChannelsCalciumCalcium ChannelsCalpainCyclooxygenase 2 InhibitorsErbB ReceptorsProtein Tyrosine Phosphatase, Non-Receptor Type 1PTPN1 protein, humanTRPV1 protein, humanTRPV Cation Channels

Identifiers

PMID25083990
PMCPMC4151223
OpenAlexW2152170007

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.