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Cholesterol level determines viability and mitogenicity, but it does not affect sodium butyrate-dependent

S Orzechowska1, B Pajak, B Gajkowska

  • 1Department of Cell Ultrastructure, Mossakowski Medical Research Centre, Polish Academy of Sciences, Pawinskiego 5, 02-106 Warsaw, Poland.

Oncology Reports
|December 15, 2010
PubMed

Insights

Cholesterol chelators reversibly reduced cancer cell survival, while NaB potentiated TNF-α-induced cell death, indicating lipid rafts are not involved in NaB-dependent cell death.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Pharmacology

Background:

  • Lipid rafts (LRs) are membrane microdomains crucial for cellular signaling.
  • Cholesterol depletion affects LR integrity and function.
  • Tumor necrosis factor-alpha (TNF-α) signaling is implicated in cancer cell survival and apoptosis.

Purpose of the Study:

  • To investigate the role of lipid rafts in human adenocarcinoma COLO 205 cell response to metabolic inhibitors and anti-cancer drugs.
  • To evaluate the effects of cholesterol depletion and replenishment on cell viability and TNF-α signaling.
  • To determine the involvement of LRs in NaB-induced cell death and its potentiation by TNF-α.

Main Methods:

  • Treatment of COLO 205 cells with lipid raft modulators (MβCD, NY, IMP) and cholesterol conjugates.
  • Challenge with metabolic inhibitors and anti-cancer drugs (CIS, CLA, EGCG, NaB).
  • Analysis of cell viability, mitogenicity, and expression of apoptotic proteins.
  • Electron microscopy (TEM, SEM) to observe cellular localization of LR-associated molecules (ceramides, Gαi-2, TNF-R1).

Main Results:

  • Cholesterol chelators reversibly reduced cell survival.
  • NaB reduced cell survival and potentiated TNF-α-induced cell death.
  • TNF-R1 clustering on the cell surface was observed and modulated by TNF-α and IMP.
  • Combined NaB and TNF-α treatment altered pro- and antiapoptotic protein expression.
  • Lipid rafts were found not to participate in NaB-dependent cell death.

Conclusions:

  • Initial prosurvival signals can be diminished by cholesterol chelators.
  • LR-independent cell survival can be targeted by NaB.
  • NaB-induced cell death is independent of lipid raft integrity.

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