Caffeic Acid Phenethyl Ester Triggers Apoptosis Through Induction of Loss of Mitochondrial Membrane Potential in Ccrf-Cem Cells

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Abstract

Purpose CAPE (caffeic acid phenethyl ester) is one of the most valuable and investigated component of propolis which is composed by honeybees. In the current study, we aimed at examining apoptotic effects of CAPE on CCRF-CEM leukemic cells and at determining the roles of mitochondrial membrane potential (MMP) in cell death. Methods Trypan blue and XTT methods were used to evaluate the cytotoxicity. Apoptosis was examined by ELISA-based oligonucleotide and acridine orange/ethidium bromide dye techniques. Loss of mitochondrial membrane potential was evaluated using JC-1 dye by flow cytometric analysis and under fluorescent microscope. Results We detected the time-and dose-dependent increases in cytotoxic effect of CAPE on CCRF-CEM cells. ELISA and acridine orange/ethidium bromide results showed that apoptotic cell population increased significantly in CCRF-CEM cells exposed to increasing concentrations of CAPE. On the other hand, there was significant loss of MMP determined in response to CAPE in CCRF-CEM cells. Conclusion This in vitro data by being supported with clinical data may open the way of the potential use of CAPE for the treatment of leukemia.

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Keywords

Apoptosis, Mitochondrial membrane potential, Cytotoxicity, Membrane Potential, Mitochondrial, Cell Death, Cytotoxicity, Antineoplastic Agents, Apoptosis, Enzyme-Linked Immunosorbent Assay, Phenylethyl Alcohol, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Flow Cytometry, CAPE, Caffeic Acids, Cell Line, Tumor, Humans, Mitochondrial membrane potential, ALL, Cell Proliferation

Fields of Science

0301 basic medicine, 0303 health sciences, 03 medical and health sciences

Citation

Avcı, Ç. B., Gündüz, C., Baran, Y., Şahin, F., Yılmaz, S., Doğan, Z. Ö., and Saydam, G.(2011). Caffeic acid phenethyl ester triggers apoptosis through induction of loss of mitochondrial membrane potential in CCRF-CEM cells. Journal of Cancer Research and Clinical Oncology, 137, 41–47. doi:10.1007/s00432-010-0857-0

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137

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41

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47
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898

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504

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