Related Experiment Video

Updated: May 23, 2026

Monitoring Hippo Signaling Pathway Activity Using a Luciferase-based Large Tumor Suppressor (LATS) Biosensor
07:16

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Published on: September 13, 2018

A lipid brake on oncogenic signaling: 13-S-HODE inhibits mTOR activity

Pallob Barai1, Jie Chen2

  • 1Department of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, Urbana, IL, USA.

Cell Chemical Biology
|May 21, 2026
PubMed

Insights

Dietary linoleic acid metabolite 13-S-hydroxyoctadecaenoic acid (13-S-HODE) inhibits mTORC1 and mTORC2 signaling. This finding provides a new mechanism for the tumor-suppressive effects of this lipid metabolite.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • The mechanistic target of rapamycin (mTOR) pathway is a central regulator of cell growth, proliferation, and metabolism.
  • Dysregulation of mTOR signaling is implicated in various cancers.
  • Dietary lipids and their metabolites can influence cellular signaling pathways, including mTOR.

Purpose of the Study:

  • To identify novel inhibitors of mTOR signaling.
  • To elucidate the molecular mechanisms underlying the tumor-suppressive activity of lipid metabolites.

Main Methods:

  • Biochemical assays to determine ATP-competitive inhibition.
  • Cellular signaling pathway analysis (mTORC1 and mTORC2).
  • In vitro and in vivo tumor models.

Main Results:

  • 13-S-hydroxyoctadecaenoic acid (13-S-HODE), a metabolite of linoleic acid, was identified as an ATP-competitive inhibitor of mTOR.
  • 13-S-HODE effectively inhibits both mTORC1 and mTORC2 signaling pathways.
  • Demonstrated tumor-suppressive activity of 13-S-HODE in preclinical models.

Conclusions:

  • 13-S-HODE is a novel dietary lipid-derived inhibitor of mTOR.
  • Inhibition of mTORC1/mTORC2 by 13-S-HODE provides a mechanistic basis for its observed tumor-suppressive effects.
  • This discovery opens new avenues for therapeutic strategies targeting lipid metabolism in cancer treatment.

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