58 Disrupting metabolic plasticity in glioblastoma stem-like cells via FABP7 inhibition and DHA supplementation

Clicks: 24
ID: 326725
2026
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Steady

Ranked #82 of 286 articles by views in journal of neuro-oncology

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 286 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Abstract
Abstract Introduction Glioblastoma (GBM) is a brain cancer with high recurrence and poor remission rates despite intensive therapies. Treatment resistance is attributed to GBM stem-like cells (GSCs), which display high metabolic plasticity to adapt to environmental and therapeutic stress. GSCs express high levels of fatty acid-binding protein 7 (FABP7), which facilitates intracellular lipid transport. FABP7 binds docosahexaenoic acid (DHA), a polyunsaturated fatty acid with anti-tumorigenic properties in GSCs. However, the GBM microenvironment is relatively low in DHA, and high FABP7 expression under these conditions contributes to an aggressive phenotype. Methods This study examines whether FABP7 inhibition and DHA supplementation disrupt metabolic plasticity in GSCs. We performed untargeted metabolomics and lipidomics in patient-derived GSCs, followed by high-resolution respirometry to assess changes in energy production. Metabolic shifts were further validated by measuring key genes and proteins involved in energy and lipid metabolism. Results Metabolomics revealed depletion of amino acids following DHA supplementation, an effect further enhanced by FABP7 inhibition. This was accompanied by increased expression of amino acid metabolism genes, suggesting a shift towards amino acids for energy production when FABP7 function is impaired. Consistently, respirometry demonstrated that FABP7 inhibition shifted mitochondrial respiration toward NADH oxidation, a key entry point for amino acid-derived substrates. Lipidomics revealed an FABP7-dependent increase in DHA-containing cholesterol esters upon DHA supplementation. We observed an FABP7-dependent decrease in the expression of ABCA1, a cholesterol efflux protein, upon DHA supplementation. As ABCA1 correlates with poor prognosis and exhibits drug efflux properties, this downregulation in ABCA1 suggests a mechanism for the anti-tumorigenic properties of DHA. Conclusion We show alterations in amino acid and lipid metabolism following FABP7 inhibition and DHA supplementation, highlighting metabolic vulnerabilities that may be therapeutic targets in glioblastoma.
Reference Key
openalex_W7204455833 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors
Journal journal of neuro-oncology
Year 2026
DOI
10.1093/neuonc/noag172.051
URL
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

No comments yet. Be the first to comment on this article.