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Gene Deletion of Microsomal Prostaglandin E Synthase-1 Suppresses Chemically Induced Skin Carcinogenesis

Yuka Sasaki1, Hiroshi Kuwata1, Eri Aida1

  • 1Division of Health Chemistry, Department of Healthcare and Regulatory Sciences, School of Pharmacy, Showa University, Tokyo, Japan.

Anticancer Research
|March 31, 2021
PubMed
Abstract

Insights

Microsomal prostaglandin E synthase-1 (mPGES-1) deficiency suppressed skin carcinogenesis in mice. This suggests mPGES-1 inhibition could be a therapeutic strategy for skin cancer.

Area of Science:

  • Biochemistry
  • Oncology
  • Inflammation Research

Background:

  • Microsomal prostaglandin E synthase-1 (mPGES-1) is a key enzyme in prostaglandin E2 (PGE2) synthesis.
  • mPGES-1 is highly expressed in various cancer types, indicating a potential role in tumorigenesis.

Purpose of the Study:

  • To investigate the role of mPGES-1 in skin carcinogenesis.
  • To determine the effect of mPGES-1 deficiency on chemically induced skin cancer development in mice.

Main Methods:

  • A two-stage skin carcinogenesis model was employed using 7,12-dimethylbenz[a]anthracene (DMBA) and 12-O-tetradecanoylphorbol-13-acetate (TPA).
  • Experiments were conducted on mPGES-1 knockout (KO) mice and their wild-type littermates on a Balb/c background.

Main Results:

  • Skin carcinogenesis induced by DMBA/TPA was significantly suppressed in mPGES-1 KO mice.
  • The induction of Interleukin-17 (IL-17) and other inflammatory cytokines by TPA was reduced in mPGES-1 deficient mice.
  • DMBA-induced apoptosis remained unaffected by mPGES-1 deficiency.

Conclusions:

  • mPGES-1 promotes chemically induced skin carcinogenesis, particularly during the promotion phase mediated by TPA.
  • Targeting mPGES-1 could represent a viable therapeutic approach for treating skin cancer.
Keywords:
inflammationmPGES-1prostaglandin E2skin carcinogenesis

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