Taxol cytotoxicity on human leukemia cell lines is a function of their susceptibility to programmed cell death

Rosaria M R Gangemi, Micaela Tiso, Carla Marchetti, Antonio Bargellesi Severi, Marina Fabbi

Research output: Contribution to journalArticlepeer-review

Abstract

Taxol is the prototype of a class of antineoplastic drugs that target microtubules. It enhances tubulin-monomer polymerization and stabilizes tubulin polymers, increasing the fraction of cells in the G2 or M phase of the cell cycle. We report that treatment of HL-60 and U937 myeloid cell lines with 1-10 μM taxol induces DNA fragmentation and the appearance of morphological features consistent with the process of apoptosis. Taxol-induced apoptosis is inhibited neither by cycloheximide nor by actinomycin D and therefore appears to be independent of new protein synthesis. Taxol causes arrest in the G2 phase of the cell cycle and affects cell viability but does not induce DNA fragmentation in the K562 erythromyeloid cell line. Protein-synthesis inhibitors, colcemid, ionomycin, and starvation, known to trigger apoptosis, proved ineffective as well. These results suggest that the antineoplastic effect of taxol is mediated in susceptible cell lines by induction of the apoptotic machinery and that K562 partial resistance may depend upon the intrinsic inability of these tumor cells to undergo apoptosis.

Original languageEnglish
Pages (from-to)385-392
Number of pages8
JournalCancer Chemotherapy and Pharmacology
Volume36
Issue number5
DOIs
Publication statusPublished - Sep 1995

Keywords

  • Apoptosis
  • Chemoresistance
  • Taxol

ASJC Scopus subject areas

  • Pharmacology
  • Oncology
  • Cancer Research

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