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Tumor suppressor RARRES1- A novel regulator of fatty acid metabolism in epithelial cells

Sara Maimouni1, Naiem Issa2, Selina Cheng2

  • 1Department of Biochemical, Molecular and Cellular Biology, Georgetown University, Washington, District of Columbia, United States of America.

Plos One
|December 18, 2018
PubMed

Insights

Retinoic acid receptor responder 1 (RARRES1) plays a key role in epithelial cell metabolism. Its depletion boosts lipid synthesis and alters glucose metabolism, impacting cell survival during starvation.

Area of Science:

  • Cellular metabolism
  • Molecular biology
  • Oncology

Background:

  • Retinoic acid receptor responder 1 (RARRES1) is implicated in cancer and metabolic disorders like hepatic steatosis, hyperinsulinemia, and obesity.
  • RARRES1 silencing is observed in numerous cancers.
  • Its precise role in metabolic reprogramming remains largely unexplored.

Purpose of the Study:

  • To elucidate the novel function of RARRES1 in the metabolic reprogramming of epithelial cells.
  • To investigate the impact of RARRES1 depletion on cellular metabolism, particularly lipid and glucose pathways.
  • To explore the therapeutic potential of targeting RARRES1 in metabolic diseases and cancer.

Main Methods:

  • Non-targeted Liquid Chromatography-Mass Spectrometry (LC-MS) to analyze metabolic changes.
  • Gene depletion studies using RARRES1 knockdown in epithelial cells.
  • Treatment with fatty acid synthase (FASN) inhibitor C75.
  • Analysis of fatty acid oxidation (FAO) and mitochondrial respiration.
  • Correlation analysis of RARRES1 expression with metabolic genes in tumors.
  • Pathway enrichment analysis focusing on peroxisome proliferating activated receptor (PPAR) signaling.

Main Results:

  • RARRES1 depletion globally increased lipid synthesis in epithelial cells.
  • Cells lacking RARRES1 shifted glucose metabolism from aerobic glycolysis to de novo lipogenesis (DNL).
  • FASN inhibition with C75 reversed the metabolic effects of RARRES1 depletion.
  • Increased DNL in RARRES1-depleted cells enhanced fatty acid availability, supporting mitochondrial respiration during starvation.
  • RARRES1 expression correlates with fatty acid metabolism genes and transcription factors in solid tumors.
  • RARRES1 is regulated by PPAR signaling.

Conclusions:

  • RARRES1 plays a critical role in regulating epithelial cell metabolism, particularly lipid synthesis and glucose utilization.
  • RARRES1-mediated metabolic reprogramming influences cell adaptation to nutrient deprivation.
  • RARRES1 is a potential therapeutic target for cancers and metabolic diseases characterized by impaired fatty acid metabolism.

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