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Updated: Jan 7, 2026

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
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Lipidomic changes in persister cancer cells drive enhanced ferroptosis sensitivity.

Eduard Reznik1, Fereshteh Zandkarimi2,3, Joleen M Csuka2

  • 1Department of Biological Sciences, Columbia University, New York, NY 10027, USA.

Ferroptosis and Oxidative Stress
|December 29, 2025
PubMed
Summary

Persister cancer cells (PSs) exhibit heightened ferroptosis sensitivity due to specific lipidomic alterations. These changes, linked to mitochondrial activity, are crucial for the survival of drug-tolerant cancer cells.

Keywords:
Polyunsaturated fatty acidcancerdiPUFAferroptosislipidsmitochondriapersisters

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Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Persister cancer cells (PSs) are drug-resistant cells that survive therapy through reversible, chromatin-mediated changes.
  • PSs are linked to minimal residual disease and cancer relapse.
  • PSs demonstrate sensitivity to ferroptosis, a key vulnerability for targeting drug-resistant cancers.

Purpose of the Study:

  • To investigate the lipidomic profiles of persister cancer cells (PSs) and their relationship with ferroptosis sensitivity.
  • To identify potential biomarkers and drivers of ferroptosis sensitivity in drug-resistant cancer cells.
  • To explore the role of mitochondria in the ferroptosis sensitivity of PSs.

Main Methods:

  • Derived PS cells (PSPC9) from lung carcinoma PC9 cells and performed transcriptomic and lipidomic analyses.
  • Reverted PSPC9 cells to a ferroptosis-resistant state (PC9PS -> PC9) to assess lipid changes.
  • Generated additional PS-like models (PSLNCaP, PSHT1080) and conducted lipidomics and mitochondrial elimination assays.

Main Results:

  • PSPC9 cells showed enriched expression of lipid and sugar metabolism genes, with increased diPUFA phospholipids (diPUFA-PL) and polyunsaturated free fatty acids (PUFA FFAs).
  • Lipid profiles reverted upon reversion of PSPC9 cells to the parental state.
  • PS-like models (LNCaP, HT1080) exhibited features of PS, including enhanced ferroptosis sensitivity and specific lipid profiles.
  • Mitochondrial elimination partially reduced ferroptosis sensitivity and altered the PS lipid profile.

Conclusions:

  • Lipidomic changes, particularly those involving diPUFA-PL and PUFA FFAs, are characteristic of ferroptosis-sensitive persister cancer cells.
  • Mitochondrial activity plays a critical role in mediating the ferroptosis sensitivity of drug-tolerant persister cancer cells.
  • Targeting these mitochondria-dependent lipidomic alterations presents a potential strategy for overcoming drug resistance in cancer.