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Role of microsomal prostaglandin E synthase-1 (mPGES-1)-derived prostaglandin E2 in colon carcinogenesis

Yuka Sasaki1, Yoshihito Nakatani1, Shuntaro Hara1

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

Prostaglandins & Other Lipid Mediators
|July 8, 2015
PubMed

Insights

Nonsteroidal anti-inflammatory drugs show promise for colorectal cancer prevention but increase cardiovascular risk. Targeting microsomal prostaglandin E synthase-1 (mPGES-1) offers an alternative strategy for cancer treatment.

Area of Science:

  • Oncology
  • Pharmacology
  • Biochemistry

Background:

  • Nonsteroidal anti-inflammatory drugs (NSAIDs), particularly selective cyclooxygenase-2 (COX-2) inhibitors, are explored for colorectal cancer chemoprevention.
  • Clinical trials reveal significant cardiovascular risks associated with these COX-2 inhibitors.
  • Microsomal prostaglandin E synthase-1 (mPGES-1) and its product PGE2 are emerging as alternative therapeutic targets.

Purpose of the Study:

  • To review the role of mPGES-1 in colon carcinogenesis.
  • To discuss the function of 15-hydroxyprostaglandin dehydrogenase (a PGE2-inactivating enzyme) in colorectal cancer.
  • To summarize the involvement of PGE2 specific receptors (EPs) in colon cancer development.

Main Methods:

  • Literature review of preclinical and clinical studies.
  • Analysis of biochemical pathways involved in prostaglandin synthesis and metabolism.
  • Examination of the expression and function of mPGES-1, 15-hydroxyprostaglandin dehydrogenase, and EP receptors in colon cancer models.

Main Results:

  • mPGES-1 and its downstream product PGE2 play a crucial role in promoting colon carcinogenesis.
  • 15-hydroxyprostaglandin dehydrogenase acts as a tumor suppressor by inactivating PGE2.
  • EP receptors mediate the pro-tumorigenic effects of PGE2 in the colon.

Conclusions:

  • Targeting the mPGES-1/PGE2 pathway presents a promising alternative to COX-2 inhibition for colorectal cancer chemoprevention and chemotherapy.
  • Modulating the activity of mPGES-1, 15-hydroxyprostaglandin dehydrogenase, and EP receptors could offer novel therapeutic strategies.
  • Further research is warranted to translate these findings into effective clinical interventions for colorectal cancer.
Keywords:
15-Hydroxyprostagladin dehydrogenaseColon carcinogenesisMicrosomal prostaglandin E synthase-1Prostaglandin E(2)Prostaglandin E(2) receptor

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