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PPARα suppresses growth of hepatocellular carcinoma in a high-fat diet context by reducing neutrophil extracellular

Banglun Pan1, Zhu Zhang1, Dongjie Ye1

  • 1Department of Hepatobiliary Surgery and Fujian Institute of Hepatobiliary Surgery, Fujian Medical University Union Hospital, Fuzhou, China.

JHEP Reports : Innovation in Hepatology
|January 13, 2025
PubMed
Summary
This summary is machine-generated.

High-fat diets promote hepatocellular carcinoma (HCC) by triggering neutrophil extracellular traps (NETs) via impaired lipid metabolism. PPARα agonists can inhibit NETs, offering a potential therapeutic strategy for HCC.

Keywords:
NF-κBPPARαcGAS-STINGhepatocellular carcinomaneutrophil extracellular trapsoxidative stress

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Area of Science:

  • Oncology
  • Immunology
  • Metabolic Disease

Background:

  • Cellular metabolism, particularly lipid homeostasis, modulates neutrophil function in hepatocellular carcinoma (HCC).
  • Alterations in lipid metabolism are linked to neutrophil extracellular trap (NET) release during HCC progression.
  • The protumor effects of high-fat diets (HFD) on HCC and the role of NETs remain unclear.

Purpose of the Study:

  • To investigate the molecular mechanisms of NET release in HCC.
  • To explore the potential beneficial effects of PPARα agonists on the HCC microenvironment.
  • To elucidate the interplay between NETs, lipid metabolism, and leukocyte interactions in HCC.

Main Methods:

  • Proteomics, metabolomics, tissue microarray, immunofluorescence, flow cytometry, western blot, and dual-luciferase reporter gene assays were employed.
  • Studies focused on the molecular pathways of NET release and PPARα signaling.
  • Preclinical models were utilized to assess the impact of PPARα agonists.

Main Results:

  • PPARα signaling was notably inhibited in HCC, with disrupted PPARα-mediated lipid metabolism driving NET release.
  • HFD induced mitochondrial impairment in neutrophils, leading to cGAS-STING activation by oxidized mitochondrial DNA (Ox-mtDNA).
  • NETs containing Ox-mtDNA were released via NLRP3-GSDMD-N in a NF-κB-dependent manner, isolating cytotoxic leukocytes from HCC.

Conclusions:

  • This study reveals a link between lipid metabolism disorders and the tumor-promoting function of NETs in HCC.
  • PPARα and its agonists are identified as therapeutic targets for managing NETs in the context of high lipid metabolism.
  • Targeting PPARα may limit NET release, enhance anti-tumor leukocyte interactions, and restrict HCC growth.