Involvement of Bax, Bcl-2, Ca2+ and caspase-3 in capsaicin-induced apoptosis of human leukemia HL-60 cells

Mei Fen Tsou, Hsu Feng Lu, Ssu Ching Chen, Lii Tzu Wu, Yi Shuan Chen, Hsiu Maan Kuo, Song Shei Lin, Jing Gung Chung

Research output: Contribution to journalArticlepeer-review

48 Scopus citations

Abstract

The role of Ca2+ on the effects of capsaicin on human leukemia HL-60 cells in vitro and the molecular mechanisms of capsaicin-induced apoptosis were investigated. The flow cytometric analysis indicated that capsaicin decreased the percentage of viable HL-60 cells, via the induction of G 0/G1-phase cell cycle arrest and apoptosis. Capsaicin-induced G0/G1-phase arrest involved the suppression of CDK2 and the cyclin E complex, which are check-point enzymes for cells moving from G0/G1- to S-phase. Capsaicin-induced apoptosis was associated with the elevation of intracellular reactive oxygen species and Ca2+ production, decreased the levels of mitochondrial membrane potential, promoted cytochrome c release and increased the activation of caspase-3. An intracellular Ca2+ chelator (BAPTA) significantly inhibited capsaicin-induced apoptosis. Capsaicin-induced apoptosis was time-and dose-dependent. These results suggest that the capsaicin-induced apoptosis of HL-60 cells may result from the activation of caspase-3 and the intracellular Ca2+ release pathway.

Original languageEnglish
Pages (from-to)1965-1971
Number of pages7
JournalAnticancer Research
Volume26
Issue number3 A
StatePublished - May 2006

Keywords

  • Apoptosis
  • Calcium
  • Capsaicin
  • Cell cycle
  • HL-60

Fingerprint

Dive into the research topics of 'Involvement of Bax, Bcl-2, Ca<sup>2+</sup> and caspase-3 in capsaicin-induced apoptosis of human leukemia HL-60 cells'. Together they form a unique fingerprint.

Cite this