11β-Prostaglandin F2α, a bioactive metabolite catalyzed by AKR1C3, stimulates prostaglandin F receptor and induces slug expression in breast cancer

Tomomi Yoda, Kyoko Kikuchi, Yasuhiro Miki, Yoshiaki Onodera, Shuko Hata, Kiyoshi Takagi, Yasuhiro Nakamura, Hisashi Hirakawa, Takanori Ishida, Takashi Suzuki, Noriaki Ohuchi, Hironobu Sasano, Keely May McNamara

Research output: Contribution to journalArticlepeer-review

15 Citations (Scopus)

Abstract

Prostaglandins are a group of lipid compounds involved in inflammation and cancer. We focused on PGF2α and its stereoisomer 11β-PGF2α and examined the expression and functions of their cognate receptor (FP receptor) and metabolizing enzymes (AKR1B1 and AKR1C3 respectively) in breast cancer. In immunohistochemical analysis FP receptor status associated with adverse clinical outcome only in the AKR1C3 positive cases. Therefore, we studied FP receptor-mediated functions of 11β-PGF2α using FP receptor expressed MCF-7 cell line (MCF-FP). 11β-PGF2α treatment phosphorylated ERK and CREB and induced Slug expression through FP receptor in MCF-FP, and MCF-FP cells demonstrated decreased chemosensitivity compared to parental controls. Finally, the correlation between FP receptor and Slug was also confirmed immunohistochemically in breast cancer cases. Overall these results indicated that the actions of AKR1C3 can produce FP receptor ligands whose activation results in carcinoma cell survival in breast cancer.

Original languageEnglish
Pages (from-to)236-247
Number of pages12
JournalMolecular and Cellular Endocrinology
Volume413
DOIs
Publication statusPublished - 2015 Sep 5

Keywords

  • 11β-Prostaglandin F2α
  • Aldo-keto reductase family 1 member C3
  • Breast cancer
  • In vitro models
  • Pathology
  • Prostaglandin F receptor
  • Slug

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology

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