Journal
EUROPEAN JOURNAL OF PHARMACOLOGY
Volume 652, Issue 1-3, Pages 23-32Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2010.11.018
Keywords
Gambogenic acid; CNE-1 cells; Apoptosis; Akt; Mitochondrial oxidative stress
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Funding
- National Science & Technology Pillar Program, China [2009ZX09103-399]
- Key Laboratory of Traditional Chinese Medicine Resource and Compound Prescription (HUCM), Ministry of Education
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In the present study, Gambogenic acid exhibits potential anti-tumor activity in several cancer cell lines. However, Gambogenic acid-induced apoptosis mechanism is not well understood. Here, we report that Gambogenic acid was capable to induce CNE-1 cells apoptosis and caused mitochondrial and endoplasmic reticulum injury, analyzed via transmission electron microscopy and acridine orange/ethidium bromide (AO/EB) double staining. To quantitatively analyze apoptosis, through the propidium iodide (PI)/Annexin V-FITC double staining to detect cell apoptosis. PI staining of the cell cycle distribution. To further explore the potential mechanism of Gambogenic acid mediated apoptosis in CNE-1 cells, we also examined mitochondrial oxidative stress in the levels of reactive oxygen species, the release of cytochrome c, intracellular Ca2+ concentration and mitochondrial membrane potential by flow cytometry. Moreover, Gambogenic acid could result in a time and concentration-dependent decrease in Phospho-Akt expression, basal expression levels of Akt change was not obvious, In addition, we detected Bcl-2 family including Bcl-2, Bax and Bad expression in mRNA level. This resulted in a decrease of Bcl-2 and Bad increased in CNE-1 cells after Gambogenic acid treatment. Overall, our results indicated that Gambogenic acid mediated apoptosis through inactivation of Akt, accompanied with mitochondrial oxidative stress and crosstalk with Bcl-2 family in the process of apoptosis. (C) 2010 Elsevier B.V. All rights reserved.
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