Cell survival or apoptosis: rooperol's role as anticancer agent

Oncol Res. 2010;18(8):365-76. doi: 10.3727/096504010x12644422320627.

Abstract

Nontoxic hypoxoside, isolated from Hypoxis, is converted to cytotoxic rooperol in the presence of beta-glucosidase. In this study, we investigated rooperol's mechanism of action. IC50 values of hypoxoside and rooperol were determined against the HeLa, HT-29, and MCF-7 cancer cell lines, and peripheral blood mononuclear cells. DNA cell cycle arrest occurred in late G1 and/or early S phases, associated with increased p21(Waf1/Cip1) levels. Apoptosis was shown by caspase-3 and/or caspase-7 activation, phosphatidylserine translocation, DNA fragmentation, cell blebbing, and apoptotic body formation. Increased phospho-Akt, phospho-Bcl-2, and p21(Waf1/Cip1) proteins, and cell size correspond to cell survival strategies (associated with endoreduplication).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alkynes / pharmacology
  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Caspase 3 / metabolism
  • Caspase 7 / metabolism
  • Catechols / pharmacology*
  • Cell Cycle / drug effects
  • Cell Line, Tumor
  • Cell Survival / drug effects*
  • DNA Fragmentation / drug effects
  • Glucosides / pharmacology
  • Humans
  • Microscopy, Phase-Contrast
  • Phosphatidylserines / metabolism

Substances

  • Alkynes
  • Antineoplastic Agents
  • Catechols
  • Glucosides
  • Phosphatidylserines
  • hypoxoside
  • rooperol
  • Caspase 3
  • Caspase 7