Polyethylene glycol induces apoptosis in HT-29 cells: potential mechanism for chemoprevention of colon cancer

FEBS Lett. 2001 May 11;496(2-3):143-6. doi: 10.1016/s0014-5793(01)02420-6.

Abstract

Recent experimental evidence suggests that polyethylene glycol (PEG) is a highly effective chemopreventive agent against colon cancer; however, the mechanism(s) remain largely unexplored. To further elucidate this issue, we evaluated the effect of PEG on two human colon cancer cell lines. PEG treatment resulted in a dose- and time-dependent reduction in cell number without alteration in markers of cell proliferation. However, there was a dramatic and specific, concentration-dependent induction of apoptosis, with 50 mM PEG rendering approximately half the cells apoptotic. This corresponded with a 17-fold induction in the expression of the pro-apoptotic protein, prostate apoptosis response-4. Our data suggest that induction of apoptosis may be responsible, at least in part, for the ability of PEG to prevent experimental colon cancer.

MeSH terms

  • Apoptosis / drug effects*
  • Apoptosis Regulatory Proteins
  • Blotting, Western
  • Carrier Proteins / metabolism
  • Cell Division / drug effects
  • Cell Separation
  • Cell Survival / drug effects
  • Colonic Neoplasms / prevention & control*
  • Coloring Agents / pharmacology
  • DNA Fragmentation
  • Dose-Response Relationship, Drug
  • Flow Cytometry
  • HT29 Cells
  • Humans
  • Intracellular Signaling Peptides and Proteins*
  • Polyethylene Glycols / pharmacology*
  • Tetrazolium Salts / pharmacology
  • Thiazoles / pharmacology
  • Time Factors
  • Tumor Cells, Cultured

Substances

  • Apoptosis Regulatory Proteins
  • Carrier Proteins
  • Coloring Agents
  • Intracellular Signaling Peptides and Proteins
  • Tetrazolium Salts
  • Thiazoles
  • prostate apoptosis response-4 protein
  • Polyethylene Glycols
  • thiazolyl blue