Related Experiment Video

Updated: Jan 29, 2026

Preparation, Purification, and Use of Fatty Acid-containing Liposomes
10:43

Preparation, Purification, and Use of Fatty Acid-containing Liposomes

Published on: February 9, 2018

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Fatty Acid Synthase as a Potential Metabolic Vulnerability in Ocular Adnexal Sebaceous Carcinoma

Autumn Berlied1, Isabella Boyack1, Andre Vieira2,3

  • 1Department of Comparative Pathobiology, Tufts University Cummings School of Veterinary Medicine, North Grafton, MA 01536, USA.

Cancers
|January 28, 2026
PubMed

Insights

Targeting fatty acid synthase (FASN) in ocular adnexal sebaceous carcinoma (SebCA) reduces cancer cell growth and alters lipid metabolism. This study reveals FASN as a potential therapeutic target for this aggressive malignancy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Ocular adnexal sebaceous carcinoma (SebCA) is an aggressive cancer with frequent MYC dysregulation.
  • Fatty acid synthase (FASN) and lipid metabolism are often altered in MYC-driven tumors, but their specific roles in SebCA are unclear.

Purpose of the Study:

  • To investigate the effects of FASN inhibition on MYC expression, SebCA cell behavior, and lipid profiles.
  • To explore the therapeutic potential of targeting FASN in SebCA.

Main Methods:

  • In vitro studies using human Meibomian gland epithelial cells and SebCA cell lines.
  • In vivo studies utilizing a MYC-overexpressing mouse model of SebCA.
  • Assessment of cell viability, proliferation, clonogenicity, lipid profiles, and gene expression.

Main Results:

  • FASN inhibition decreased SebCA cell viability, proliferation, and clonogenicity.
  • FASN inhibition altered fatty acid saturation in various lipid classes, notably ceramides.
  • MYC overexpression promoted proliferation and suppressed differentiation in a mouse model, effects exacerbated by FASN inhibition.

Conclusions:

  • MYC expression in SebCA is sensitive to FASN inhibition.
  • Targeting FASN represents a metabolic vulnerability and a potential therapeutic strategy for SebCA.
Keywords:
C75MYCMeibomian gland (MG)apoptosisceramidedifferentiationfatty acidmass spectrometryproliferationsaturation

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