Fatty acid 2-hydroxylase (FA2H) as a stimulatory molecule responsible for breast cancer cell migration

Masayo Hirao-Suzuki, Takayuki Koga, Genki Sakai, Takanobu Kobayashi, Yuji Ishii, Hiroshi Miyazawa, Masufumi Takiguchi, Narumi Sugihara, Akihisa Toda, Masahiro Ohara, Shuso Takeda

Research output: Contribution to journalArticlepeer-review

Abstract

The functional role of fatty acid 2-hydroxylase (FA2H) is controversial in the field of cancer biology due to the dual role of FA2H, particularly related to its interaction with triple-negative breast cancer (TNBC). A previous biochemical- and clinical-focused study suggested that FA2H could dampen TNBC aggressiveness. However, another epidemiological study demonstrated that FA2H expression is associated with shorter disease-free survival in TNBC cases. We reported that FA2H is a peroxisome proliferator-activated receptor α (PPARα)-regulated gene in human breast cancer MDA-MB-231 cells, in vitro experimental models for TNBC analysis. PPARα activation by its ligand reportedly results in an aggressive MDA-MB-231 cell phenotype, as well as estrogen receptor α (ERα)-positive MCF-7 cells. The results of this study show that i) MDA-MB-231 cells express very low levels of FA2H compared to the MCF-7 cells, reflecting a low basal-level PPARα-driven transcriptional activity compared to the MCF-7 cells, and ii) the increased FA2H expression stimulates the MDA-MB-231 and MCF-7 breast cancer cell migration without affecting proliferation. Taken together, our findings indicate that FA2H might be a breast cancer cell migration stimulator, independently of the ERα expression status.

Original languageEnglish
Pages (from-to)215-222
Number of pages8
JournalBiochemical and Biophysical Research Communications
Volume531
Issue number2
DOIs
Publication statusPublished - Oct 15 2020

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Fingerprint Dive into the research topics of 'Fatty acid 2-hydroxylase (FA2H) as a stimulatory molecule responsible for breast cancer cell migration'. Together they form a unique fingerprint.

Cite this