Cookies Policy

This site uses cookies. By continuing to browse the site you are agreeing to our use of cookies.

I accept this policy

Find out more here

Effect of BCL-2 on Harringtonine-induced apoptosis and intracellular Ca2+ mobilization in human leukemia HL-60 cells

No metrics data to plot.
The attempt to load metrics for this article has failed.
The attempt to plot a graph for these metrics has failed.
The full text of this article is not currently available.

Brill’s MyBook program is exclusively available on BrillOnline Books and Journals. Students and scholars affiliated with an institution that has purchased a Brill E-Book on the BrillOnline platform automatically have access to the MyBook option for the title(s) acquired by the Library. Brill MyBook is a print-on-demand paperback copy which is sold at a favorably uniform low price.

This Article is currently unavailable for purchase.
Add to Favorites
You must be logged in to use this functionality

Cover image Placeholder

Harringtonine (HT), a kind of anticancer drug isolated from Chinese herb Cephalotaxus hainanensis Li, has been used in the clinical treatment of human glanulocytic leukemia and chromic myelocytic leukemia. In this study, we investigated the effect of Bcl-2 on HT-induced apoptosis and Ca2+ mobilization in human leukemia HL-60 cells. 1 μg/ml HT induced the apoptosis of HL-60/Neo cells in a time-dependent manner; while 1 μg/ml HT failed to induce the apoptosis of HL-60/ Bcl-2 cells. HT-, A23187- (a Ca2+ ionophore), Carbonyl cyanide m-chlorophenylhydrazone (CCCP,a specific releaser of Ca2+ from mitochondria) and thapsigargin- (an inhibitor of endoplasmic reticulum Ca2+>-ATPase) induced changes in [Ca2+]i were monitored by using Fluo 3-AM with confocal laser scanning microscopy. The results demonstrated that HL-60 cells with enforced expression of Bcl-2 (HL-60/Bcl-2 cells) had increased Ca2+ permeability and increased intracellular Ca2+ store in comparison with HL-60 cells with negative control vectors (HL-60/Neo cells), suggesting that Bcl-2 might prevent HT-induced apoptosis by increased Ca2+ permeability and increased intracellular Ca2+ buffering capacity.


Full text loading...


Data & Media loading...

Article metrics loading...



Can't access your account?
  • Key

  • Full access
  • Open Access
  • Partial/No accessInformation