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ORMDL2 Promotes the Growth of Glioma through mTORC1-Mediated Fatty Acid Metabolism

  • 0Department of Neurosurgery, Yantaishan Hospital Affiliated to Binzhou Medical University, No. 10087, Keji Avenue, Laishan District, Yantai, 264003, Shandong, China.
Applied Biochemistry and Biotechnology +

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September 2, 2025

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September 2, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

ORMDL sphingolipid biosynthesis regulator 2 (ORMDL2) is highly expressed in glioma, promoting tumor growth by activating mTORC1-mediated fatty acid metabolism. Silencing ORMDL2 inhibits glioma progression and improves survival rates.

Area Of Science

  • Oncology
  • Molecular Biology
  • Biochemistry

Background

  • Fatty acid metabolism is crucial in glioma pathogenesis.
  • The role of ORMDL sphingolipid biosynthesis regulator 2 (ORMDL2) in glioma's fatty acid metabolism requires investigation.

Purpose Of The Study

  • To investigate the role of ORMDL2 in glioma cell fatty acid metabolism.
  • To determine the association between ORMDL2 expression and glioma patient survival.

Main Methods

  • Analysis of The Cancer Genome Atlas (TCGA) data and Kaplan-Meier survival curves.
  • In vitro studies using human glioma cells and in vivo mouse glioma models.
  • Assessment of cell proliferation, apoptosis, and fatty acid metabolism via CCK-8, flow cytometry, BODIPY staining, Western blotting, and qRT-PCR.

Main Results

  • ORMDL2 was upregulated in glioma tissues and associated with poor survival.
  • ORMDL2 silencing inhibited glioma cell proliferation, promoted apoptosis, and reduced lipid droplet formation.
  • Tumor growth was inhibited in mice with ORMDL2 silencing.
  • ORMDL2 silencing decreased fatty acid metabolism factors (FASN, ACC1, SCD1) and mTORC1/S6K phosphorylation.

Conclusions

  • ORMDL2 is overexpressed in glioma and promotes tumor progression.
  • ORMDL2 activates mTORC1-mediated fatty acid metabolism in glioma cells.
  • Targeting ORMDL2 may represent a therapeutic strategy for glioma.

Keywords:

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