Apoptosis and cytolysis induced by giganteosides and hederacolchisides in HL-60 cells

Pascal C. Gerkens, Rowan Dobson, Nino Tabatadze, Vakhtang Mshviladzade, Riad Elias, Olivier J. Peulen, Olivier M. Jolois, Marie Claire A De Pauw-Gillet

Research output: Contribution to journalArticlepeer-review

13 Scopus citations


The viability, cytolysis and apoptosis-mediated cellular death induced by giganteosides D and E (Gig-D and Gig-E) and hederacolchisides A and A1 (Hcol-A and Hcol-A1) were analysed in HL-60 cells. Materials and Methods: The end-point metabolic (WST1) and lactate dehydrogenase (LDH) assays were used. Cell cycle analysis and apoptosis were measured by flow cytometry, DNA laddering and caspase-3 analyses. Results: the HL-60 cell line was more sensitive to Hcol-A1 and Gig-D (IC50 3-5 μM) than to Gig-E and Hcol-A (IC50 8-13 μM; WST1 assay). This was related to LDH release. The induction of apoptosis could be detected without caspase-3 activation after 24 h of treatment. DNA fragmentation could be detected only with Gig-D. With Hcol-A1 and Gig-D, an accumulation of cells in the S-phase and an increase of cells in sub-G1 peak were observed. By the annexinV-fluorescein isothiocyanate (FITC)/7-amino-actinomycin D (AAD) assay, the majority of cells were in late apoptosis with Gig-D, and in necrosis with Hcol-A1. Conclusion: Hcol-A1 is more cytotoxic than Gig-D, followed by Gig-E and finally Hcol-A. This is related to a membrane permeabilization effect, leading to cytolysis.

Original languageEnglish (US)
Pages (from-to)2529-2534
Number of pages6
JournalAnticancer Research
Issue number4 B
StatePublished - Jul 1 2007


  • Apoptosis
  • Cytolysis
  • Giganteoside
  • Hederacolchiside
  • HL-60

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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