Different regulatory pathways are involved in the proliferative inhibition of two types of leukemia cell lines induced by paclitaxel

Oncol Rep. 2013 Oct;30(4):1853-9. doi: 10.3892/or.2013.2624. Epub 2013 Jul 18.

Abstract

Paclitaxel, one of the broadest-spectrum anticancer agents, is currently being used in the treatment of patients with solid tumors. In the present study, we compared the effect of paclitaxel on two types of leukemia cells. Our results showed that paclitaxel could inhibit the proliferation of MEL and K562 cells in a dose- and time-dependent manner. The mechanism of proliferative inhibition in K562 cells treated by paclitaxel was related to the cell cycle arrest in the G2/M phase, as well as the induction of apoptosis. By contrast, MEL cells treated by paclitaxel showed significant characteristics of necrosis, which indicated that the mode of cell death induced by paclitaxel in these two types of leukemia cells differed. Advances in research of the cell cycle, apoptosis and necrosis will extend our understanding of the mechanisms of paclitaxel-induced cell death, particularly in leukemia cells. Further elucidation of the mechanisms of necrosis in MEL cells may expedite the development of improved paclitaxel-based regimens for cancer therapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents, Phytogenic / pharmacology*
  • Apoptosis / drug effects*
  • Cell Division / drug effects
  • Cell Line, Tumor
  • Cell Proliferation
  • Humans
  • Leukemia / drug therapy*
  • Leukemia / metabolism
  • M Phase Cell Cycle Checkpoints / drug effects*
  • Paclitaxel / pharmacology*

Substances

  • Antineoplastic Agents, Phytogenic
  • Paclitaxel