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Apoptosis-inducing active components from Corbicula fluminea through activation of caspase-2 and production of reactive oxygen species in human leukemia HL-60 cells.
Food Chem Toxicol. 2006 Aug; 44(8):1261-72.FC

Abstract

The anti-cancer effects and possible mechanisms of the freshwater clam (Corbicula fluminea Muller) and its active compounds (FME) on cell viability in human leukemia HL-60 cells were investigated. This study demonstrated that FME was able to inhibit cell proliferation in a concentration- and time-dependent manner. Treatment with FME caused induction of caspase-2, caspase-3, caspase-6, caspase-8, and caspase-9 activity in a time-dependent manner, but not affect caspase-1 activity; it induced the proteolysis of DNA fragmentation factor (DFF-45) and poly(ADP-ribose) polymerase (PARP). Induction of cell death by FME was completely prevented by a pan-caspase inhibitor, Z-Val-Ala-Asp-fluoromethyl ketone (Z-VAD-FMK) and a caspase-2 inhibitor, Z-Val-Asp-Val-Ala-Asp-FMK (Z-VDVAD-FMK). Furthermore, treatment with FME caused a rapid loss of mitochondrial transmembrane potential, stimulation of generation of reactive oxygen species (ROS), release of mitochondrial cytochrome c into cytosol, and GSH depletion. Anti-oxidants such as N-acetylcysteine, catalase, superoxide dismutase, allopurinol, and pyrrolidine dithiocarbamate, but not diphenylene iodonium, significantly inhibited FME-induced cell death. In addition, the results showed that FME-induced apoptosis was accompanied by up-regulation of Bax and Bad, and down-regulation of Bcl-2 and Bcl-XL. Taken together, induction of apoptosis on HL-60 cells by FME was mainly associated with ROS production, GSH depletion, mitochondrial dysfunction, and caspase activation.

Authors+Show Affiliations

Department of Marine Biotechnology, National Kaohsiung Marine University, Kaohsiung, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16545898

Citation

Huang, Ying-Tang, et al. "Apoptosis-inducing Active Components From Corbicula Fluminea Through Activation of Caspase-2 and Production of Reactive Oxygen Species in Human Leukemia HL-60 Cells." Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association, vol. 44, no. 8, 2006, pp. 1261-72.
Huang YT, Huang YH, Hour TC, et al. Apoptosis-inducing active components from Corbicula fluminea through activation of caspase-2 and production of reactive oxygen species in human leukemia HL-60 cells. Food Chem Toxicol. 2006;44(8):1261-72.
Huang, Y. T., Huang, Y. H., Hour, T. C., Pan, B. S., Liu, Y. C., & Pan, M. H. (2006). Apoptosis-inducing active components from Corbicula fluminea through activation of caspase-2 and production of reactive oxygen species in human leukemia HL-60 cells. Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association, 44(8), 1261-72.
Huang YT, et al. Apoptosis-inducing Active Components From Corbicula Fluminea Through Activation of Caspase-2 and Production of Reactive Oxygen Species in Human Leukemia HL-60 Cells. Food Chem Toxicol. 2006;44(8):1261-72. PubMed PMID: 16545898.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Apoptosis-inducing active components from Corbicula fluminea through activation of caspase-2 and production of reactive oxygen species in human leukemia HL-60 cells. AU - Huang,Ying-Tang, AU - Huang,Yi-Hsuan, AU - Hour,Tzhy-Chyuan, AU - Pan,Bonnie Sun, AU - Liu,Yeuk-Chuen, AU - Pan,Min-Hsiung, Y1 - 2006/03/20/ PY - 2005/09/25/received PY - 2006/01/30/revised PY - 2006/02/01/accepted PY - 2006/3/21/pubmed PY - 2006/9/20/medline PY - 2006/3/21/entrez SP - 1261 EP - 72 JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association JO - Food Chem Toxicol VL - 44 IS - 8 N2 - The anti-cancer effects and possible mechanisms of the freshwater clam (Corbicula fluminea Muller) and its active compounds (FME) on cell viability in human leukemia HL-60 cells were investigated. This study demonstrated that FME was able to inhibit cell proliferation in a concentration- and time-dependent manner. Treatment with FME caused induction of caspase-2, caspase-3, caspase-6, caspase-8, and caspase-9 activity in a time-dependent manner, but not affect caspase-1 activity; it induced the proteolysis of DNA fragmentation factor (DFF-45) and poly(ADP-ribose) polymerase (PARP). Induction of cell death by FME was completely prevented by a pan-caspase inhibitor, Z-Val-Ala-Asp-fluoromethyl ketone (Z-VAD-FMK) and a caspase-2 inhibitor, Z-Val-Asp-Val-Ala-Asp-FMK (Z-VDVAD-FMK). Furthermore, treatment with FME caused a rapid loss of mitochondrial transmembrane potential, stimulation of generation of reactive oxygen species (ROS), release of mitochondrial cytochrome c into cytosol, and GSH depletion. Anti-oxidants such as N-acetylcysteine, catalase, superoxide dismutase, allopurinol, and pyrrolidine dithiocarbamate, but not diphenylene iodonium, significantly inhibited FME-induced cell death. In addition, the results showed that FME-induced apoptosis was accompanied by up-regulation of Bax and Bad, and down-regulation of Bcl-2 and Bcl-XL. Taken together, induction of apoptosis on HL-60 cells by FME was mainly associated with ROS production, GSH depletion, mitochondrial dysfunction, and caspase activation. SN - 0278-6915 UR - https://www.unboundmedicine.com/medline/citation/16545898/Apoptosis_inducing_active_components_from_Corbicula_fluminea_through_activation_of_caspase_2_and_production_of_reactive_oxygen_species_in_human_leukemia_HL_60_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0278-6915(06)00027-5 DB - PRIME DP - Unbound Medicine ER -