Polyphyllin D induces mitochondrial fragmentation and acts directly on the mitochondria to induce apoptosis in drug-resistant HepG2 cells

Abstract We previously showed that polyphyllin D (PD) produced a stronger apoptotic effect in R-HepG2 with multi-drug resistance (MDR) than that in its parent HepG2 cells without MDR. In this study, PD was found to elicit mitochondrial fragmentation in live cells by using total internal reflection f...

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Bibliographic Details
Published in:Cancer letters 2008-03, Vol.261 (2), p.158-164
Main Authors: Ong, Rose C.Y, Lei, Jin, Lee, Rebecca K.Y, Cheung, Jenny Y.N, Fung, K.P, Lin, Chinlon, Ho, H.P, Yu, Biao, Li, Ming, Kong, S.K
Format: Article
Language:English
Subjects:
Apoptosis
Apoptosis - drug effects
Blotting, Western
Cancer
Carcinoma, Hepatocellular - drug therapy
Carcinoma, Hepatocellular - pathology
Caspases - metabolism
Cell culture
Diosgenin - analogs & derivatives
Diosgenin - pharmacology
Drug dosages
Drug Resistance, Neoplasm
Drugs, Chinese Herbal - pharmacology
Hematology
Hematology, Oncology and Palliative Medicine
Humans
Liver Neoplasms - drug therapy
Liver Neoplasms - pathology
Membrane Potential, Mitochondrial - drug effects
Microscopy, Fluorescence
Mitochondria
Mitochondria - drug effects
Molecular weight
Multi-drug resistance
Polyphyllin D
Proteins
R-HepG2
Saponins
Total internal reflection fluorescence
Tumor Cells, Cultured
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Summary:Abstract We previously showed that polyphyllin D (PD) produced a stronger apoptotic effect in R-HepG2 with multi-drug resistance (MDR) than that in its parent HepG2 cells without MDR. In this study, PD was found to elicit mitochondrial fragmentation in live cells by using total internal reflection fluorescence microscopy (TIRFM). When mitochondria were isolated and treated directly with PD, a stronger swelling, deeper transmembrane depolarization, and more apoptosis-inducing factor (AIF) release were observed from the mitochondria of R-HepG2 than that of HepG2. These observations suggest that PD is a potent anti-cancer agent that bypasses MDR and elicits apoptosis via mitochondrial injury.
ISSN:0304-3835
1872-7980
DOI:10.1016/j.canlet.2007.11.005