Sökning: id:"swepub:oai:DiVA.org:liu-43256" >
Genetic deletion of...
Genetic deletion of mPGES-1 accelerates intestinal tumorigenesis in APCMin/+ mice
-
- Elander, Nils, 1980- (författare)
- Linköpings universitet,Cellbiologi,Hälsouniversitetet
-
- Ungerbäck, Jonas, 1982- (författare)
- Linköpings universitet,Cellbiologi,Hälsouniversitetet
-
- Olsson, Hans, 1963- (författare)
- Östergötlands Läns Landsting,Linköpings universitet,Hälsouniversitetet,Molekylär och immunologisk patologi,Klinisk patologi och klinisk genetik
-
visa fler...
-
- Uematsu, Satoshi (författare)
- Department of Host Defense, Research Institute for Microbial Diseases Osaka University, Osaka, Japan
-
- Akira, Shizuo (författare)
- Department of Host Defense, Research Institute for Microbial Diseases Osaka University, Osaka, Japan
-
- Söderkvist, Peter, 1953- (författare)
- Linköpings universitet,Hälsouniversitetet,Cellbiologi
-
visa färre...
-
(creator_code:org_t)
- Elsevier BV, 2008
- 2008
- Engelska.
-
Ingår i: Biochemical and Biophysical Research Communications - BBRC. - : Elsevier BV. - 0006-291X .- 1090-2104. ; 372:1, s. 249-253
- Relaterad länk:
-
http://www.ncbi.nlm....
-
visa fler...
-
https://urn.kb.se/re...
-
https://doi.org/10.1...
-
visa färre...
Abstract
Ämnesord
Stäng
- The induced synthesis of bioactive prostanoids downstream of cyclooxygenase-2 (COX-2) and prostaglandin H2 (PGH2) exerts a critical event in colorectal carcinogenesis. Here we demonstrate that APCMin/+ mice with genetic deletion of microsomal prostaglandin E synthase-1 (mPGES-1), which catalyses the terminal conversion of PGH2 into PGE2, surprisingly develop more and generally larger intestinal tumors than do mPGES-1 wild type littermates (mean number of tumors/intestine 80 vs. 38, p < 0.0005, mean tumor diameter 1.64 vs. 1.12 mm, p < 0.0005). No deviation regarding the expression of other PGE2 related enzymes (COX-1, COX-2, mPGES-2, cPGES, and 15-PGDH) or receptors (EP1-4) was obvious among the mPGES-1 deficient mice. PGE2 levels were suppressed in tumors of mPGES-1 deficient animals, but the concentrations of other PGH2 derived prostanoids were generally enhanced, being most prominent for TxA2 and PGD2. Thus, we hypothesise that a redirected synthesis towards other lipid mediators might (over)compensate for loss of mPGES-1/PGE2 during intestinal tumorigenesis. Nevertheless, our results question the suitability for mPGES-1 targeting therapy in the treatment or prevention of colorectal cancer. © 2008 Elsevier Inc. All rights reserved.
Nyckelord
- 6-Ketoprostaglandin F1 alpha/analysis Animals Cell Transformation
- Neoplastic/*genetics/pathology Colorectal Neoplasms/*genetics/pathology Dinoprostone/analysis/*metabolism Female *Gene Deletion Intramolecular Oxidoreductases/*genetics Male Mice Mice
- Mut
- MEDICINE
- MEDICIN
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
Hitta via bibliotek
Till lärosätets databas