NDLI: Phenethyl isothiocyanate inhibits growth of human chronic myeloid leukemia K562 cells via reactive oxygen species generation and caspases.

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Phenethyl isothiocyanate inhibits growth of human chronic myeloid leukemia K562 cells via reactive oxygen species generation and caspases.

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Phenethyl isothiocyanate inhibits growth of human chronic myeloid leukemia K562 cells via reactive oxygen species generation and caspases.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wang, Yating Wei, Sixi Wang, Jishi Fang, Qin Chai, Qixiang
Description	Author Affiliation: Wang Y ( Department of Hematology, First Affiliated Hospital of Guiyang Medical College, Guiyang, Guizhou 550004, P.R. China.); Wei S ( Department of Hematology, First Affiliated Hospital of Guiyang Medical College, Guiyang, Guizhou 550004, P.R. China.); Wang J ( Department of Hematology, First Affiliated Hospital of Guiyang Medical College, Guiyang, Guizhou 550004, P.R. China.); Fang Q ( Department of Pharmacy, First Affiliated Hospital of Guiyang Medical College, Guiyang, Guizhou 550004, P.R. China.); Chai Q ( Department of Hematology, First Affiliated Hospital of Guiyang Medical College, Guiyang, Guizhou 550004, P.R. China.)
Abstract	Phenethyl isothiocyanate (PEITC), a potential cancer chemopreventive constituent of cruciferous vegetables, including watercress, has been reported to inhibit cancer cell growth by arresting the cell cycle and inducing apoptosis in various human cancer cell models. However, the role of PEITC in the inhibition of human chronic myeloid leukemia (CML) K562 cell growth and its underlying mechanisms have yet to be elucidated. In the present study, PEITC was found to induce cell death through the induction of reactive oxygen species (ROS) stress and oxidative damage. Heme oxygenase1 (HO1), which participates in the development of numerous tumors and the sensitivity of these tumors to chemotherapeutic drugs, plays a protective role by modulating oxidative injury. Therefore, the present study assessed the inhibitory effect of PEITC on K562 cells and whether HO1 facilitated cell apoptosis and ROS generation. PEITC was found to suppress cell growth and cause apoptosis by promoting Fas and Fas ligand expression, increasing ROS generation and by the successive release of cytochrome c as well as the activation of caspase9 and caspase3. PEITC was also combined with the HO1 inhibitor zinc protoporphyrin IX and the inducer hemin to assess whether HO1 determines cell survival and ROS generation. The results of the present study suggest that PEITC may be a potential antitumor compound for CML therapy, and that HO1 has a critical function in PEITCinduced apoptosis and ROS generation.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	1
Volume Number	10
Language	English
Publisher	Spandidos Publications
Publisher Date	2014-07-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Anticarcinogenic Agents Pharmacology Apoptosis Drug Effects Caspases Metabolism Isothiocyanates Reactive Oxygen Species Caspase 3 Genetics Caspase 9 Cell Proliferation Cytochromes c Heme Oxygenase-1 K562 Cells Leukemia, Myelogenous, Chronic, Bcr-abl Positive Pathology Rna, Messenger Research Support, Non-u.s. Gov't Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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