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Erschienen in: Journal of Cancer Research and Clinical Oncology 1/2011

01.01.2011 | Original Paper

Caffeic acid phenethyl ester triggers apoptosis through induction of loss of mitochondrial membrane potential in CCRF-CEM cells

verfasst von: Çığır Biray Avcı, Cumhur Gündüz, Yusuf Baran, Fahri Şahin, Sunde Yılmaz, Zeynep Ozlem Dogan, Güray Saydam

Erschienen in: Journal of Cancer Research and Clinical Oncology | Ausgabe 1/2011

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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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Metadaten
Titel
Caffeic acid phenethyl ester triggers apoptosis through induction of loss of mitochondrial membrane potential in CCRF-CEM cells
verfasst von
Çığır Biray Avcı
Cumhur Gündüz
Yusuf Baran
Fahri Şahin
Sunde Yılmaz
Zeynep Ozlem Dogan
Güray Saydam
Publikationsdatum
01.01.2011
Verlag
Springer-Verlag
Erschienen in
Journal of Cancer Research and Clinical Oncology / Ausgabe 1/2011
Print ISSN: 0171-5216
Elektronische ISSN: 1432-1335
DOI
https://doi.org/10.1007/s00432-010-0857-0

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