Bufalin enhances TRAIL-induced apoptosis by redistributing death receptors in lipid rafts in breast cancer cells

Anticancer Drugs. 2014 Jul;25(6):683-9. doi: 10.1097/CAD.0000000000000095.

Abstract

Studies have shown that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) selectively induces apoptosis in cancer cells. However, breast cancer cells are generally resistant to TRAIL. In the present study, we explored the effect of bufalin on TRAIL-induced breast cancer cell apoptosis. The results showed that bufalin enhanced TRAIL-induced apoptosis in MCF-7 and MDA-MB-231 breast cancer cells by activating the extrinsic apoptotic pathway. Bufalin also promoted the clustering of death receptor 4 (DR4) and DR5 in aggregated lipid rafts. The cholesterol-sequestering agent methyl-β-cyclodextrin reversed the DR4 and DR5 clustering and reduced bufalin+TRAIL-induced apoptosis. Overall, these results indicate that bufalin enhanced TRAIL-induced apoptosis in breast cancer cells by the partial redistribution of DRs in lipid rafts.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology
  • Bufanolides / pharmacology*
  • Cell Line, Tumor
  • Cholesterol / metabolism
  • Female
  • Humans
  • Membrane Microdomains / metabolism*
  • Receptors, TNF-Related Apoptosis-Inducing Ligand / metabolism*
  • TNF-Related Apoptosis-Inducing Ligand / metabolism*
  • beta-Cyclodextrins / pharmacology

Substances

  • Antineoplastic Agents
  • Bufanolides
  • Receptors, TNF-Related Apoptosis-Inducing Ligand
  • TNF-Related Apoptosis-Inducing Ligand
  • beta-Cyclodextrins
  • methyl-beta-cyclodextrin
  • Cholesterol
  • bufalin