Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Transient receptor potential type vanilloid 1 suppresses skin carcinogenesis.

Cancer research | Feb 1, 2009

http://www.ncbi.nlm.nih.gov/pubmed/19155296

Blockade of the transient receptor potential channel vanilloid subfamily 1 (TRPV1) is suggested as a therapeutic approach to pain relief. However, TRPV1 is a widely expressed protein whose function might be critical in various nonneuronal physiologic conditions. The epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase that is overexpressed in many human epithelial cancers and is a potential target for anticancer drugs. Here, we show that TRPV1 interacts with EGFR, leading to EGFR degradation. Notably, the absence of TRPV1 in mice results in a striking increase in skin carcinogenesis. The TRPV1 is the first membrane receptor shown to have a tumor-suppressing effect associated with the down-regulation of another membrane receptor. The data suggest that, although a great deal of interest has focused on TRPV1 as a target for pain relief, the chronic blockade of this pain receptor might increase the risk for cancer development.

Pubmed ID: 19155296 RIS Download

Mesh terms: Animals | Carcinogens | Cell Line, Tumor | Cell Transformation, Neoplastic | Down-Regulation | Lysosomes | Mice | Mice, Knockout | Protein Structure, Tertiary | Proto-Oncogene Proteins c-cbl | Receptor, Epidermal Growth Factor | Skin Neoplasms | TRPV Cation Channels | Tetradecanoylphorbol Acetate | Ubiquitin

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

  • Agency: NCI NIH HHS, Id: CA007646
  • Agency: NCI NIH HHS, Id: CA027502
  • Agency: NCI NIH HHS, Id: CA088961
  • Agency: NCI NIH HHS, Id: CA111536
  • Agency: NCI NIH HHS, Id: CA120388
  • Agency: NCI NIH HHS, Id: P01 CA027502
  • Agency: NCI NIH HHS, Id: P01 CA027502-270022
  • Agency: NCI NIH HHS, Id: P01 CA088961
  • Agency: NCI NIH HHS, Id: P01 CA088961-020003
  • Agency: NCI NIH HHS, Id: R01 CA077646
  • Agency: NCI NIH HHS, Id: R01 CA077646-09
  • Agency: NCI NIH HHS, Id: R01 CA081064
  • Agency: NCI NIH HHS, Id: R01 CA081064-08
  • Agency: NCI NIH HHS, Id: R01 CA111536
  • Agency: NCI NIH HHS, Id: R01 CA111536-04
  • Agency: NCI NIH HHS, Id: R01 CA120388
  • Agency: NCI NIH HHS, Id: R01 CA120388-03
  • Agency: NCI NIH HHS, Id: R37 CA081064

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.