Regulation of p53-, Bcl-2- and Caspase-dependent Signaling Pathway in Xanthorrhizol-induced Apoptosis of HepG2 Hepatoma Cells

Xanthorrhizol is a sesquiterpenoid compound extracted from the rhizome of Curcuma xanthorrhiza. This study investigated the antiproliferative effect and the mechanism of action of xanthorrhizol on human hepatoma cells, HepG2, and the mode of cell death. An antiproliferative assay using methylene blu...

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Main Authors: Tri Handayani, Syed Alwi, Sharifah Sakinah, Nallappan, Meenakshii, Lope Pihie, Azimahtol Hawariah
Format: Article
Language:English
English
Published: International Institute of Anticancer Research (IIAR) 2007
Online Access:http://psasir.upm.edu.my/id/eprint/7266/
http://psasir.upm.edu.my/id/eprint/7266/1/Regulation%20of%20p53.pdf
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author Tri Handayani,
Syed Alwi, Sharifah Sakinah
Nallappan, Meenakshii
Lope Pihie, Azimahtol Hawariah
author_facet Tri Handayani,
Syed Alwi, Sharifah Sakinah
Nallappan, Meenakshii
Lope Pihie, Azimahtol Hawariah
author_sort Tri Handayani,
building UPM Institutional Repository
collection Online Access
description Xanthorrhizol is a sesquiterpenoid compound extracted from the rhizome of Curcuma xanthorrhiza. This study investigated the antiproliferative effect and the mechanism of action of xanthorrhizol on human hepatoma cells, HepG2, and the mode of cell death. An antiproliferative assay using methylene blue staining revealed that xanthorrhizol inhibited the proliferation of the HepG2 cells with a 50% inhibition of cell growth (IC50) value of 4.17±0.053 μg/ml. The antiproliferative activity of xanthorrhizol was due to apoptosis induced in the HepG2 cells and not necrosis, which was confirmed by the Tdt-mediated dUTP nick end labeling (TUNEL) assay. The xanthorrhizol-treated HepG2 cells showed typical apoptotic morphology such as DNA fragmentation, cell shrinkage and elongated lamellipodia. The apoptosis mediated by xanthorrhizol in the HepG2 cells was associated with the activation of tumor suppressor p53 and down-regulation of antiapoptotic Bcl-2 protein expression, but not Bax. The levels of Bcl-2 protein expression decreased 24-h after treatment with xanthorrhizol and remained lower than controls throughout the experiment, resulting in a shift in the Bax to Bcl-2 ratio thus favouring apoptosis. The processing of the initiator procaspase-9 was detected. Caspase-3 was also found to be activated, but not caspase-7. Xanthorrhizol exerts antiproliferative effects on HepG2 cells by inducing apoptosis via the mitochondrial pathway.
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publishDate 2007
publisher International Institute of Anticancer Research (IIAR)
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spelling upm-72662016-01-21T01:44:55Z http://psasir.upm.edu.my/id/eprint/7266/ Regulation of p53-, Bcl-2- and Caspase-dependent Signaling Pathway in Xanthorrhizol-induced Apoptosis of HepG2 Hepatoma Cells Tri Handayani, Syed Alwi, Sharifah Sakinah Nallappan, Meenakshii Lope Pihie, Azimahtol Hawariah Xanthorrhizol is a sesquiterpenoid compound extracted from the rhizome of Curcuma xanthorrhiza. This study investigated the antiproliferative effect and the mechanism of action of xanthorrhizol on human hepatoma cells, HepG2, and the mode of cell death. An antiproliferative assay using methylene blue staining revealed that xanthorrhizol inhibited the proliferation of the HepG2 cells with a 50% inhibition of cell growth (IC50) value of 4.17±0.053 μg/ml. The antiproliferative activity of xanthorrhizol was due to apoptosis induced in the HepG2 cells and not necrosis, which was confirmed by the Tdt-mediated dUTP nick end labeling (TUNEL) assay. The xanthorrhizol-treated HepG2 cells showed typical apoptotic morphology such as DNA fragmentation, cell shrinkage and elongated lamellipodia. The apoptosis mediated by xanthorrhizol in the HepG2 cells was associated with the activation of tumor suppressor p53 and down-regulation of antiapoptotic Bcl-2 protein expression, but not Bax. The levels of Bcl-2 protein expression decreased 24-h after treatment with xanthorrhizol and remained lower than controls throughout the experiment, resulting in a shift in the Bax to Bcl-2 ratio thus favouring apoptosis. The processing of the initiator procaspase-9 was detected. Caspase-3 was also found to be activated, but not caspase-7. Xanthorrhizol exerts antiproliferative effects on HepG2 cells by inducing apoptosis via the mitochondrial pathway. International Institute of Anticancer Research (IIAR) 2007 Article PeerReviewed application/pdf en http://psasir.upm.edu.my/id/eprint/7266/1/Regulation%20of%20p53.pdf Tri Handayani, and Syed Alwi, Sharifah Sakinah and Nallappan, Meenakshii and Lope Pihie, Azimahtol Hawariah (2007) Regulation of p53-, Bcl-2- and Caspase-dependent Signaling Pathway in Xanthorrhizol-induced Apoptosis of HepG2 Hepatoma Cells. Anticancer Research, 27 (2). pp. 965-972. ISSN 0250-7005 http://ar.iiarjournals.org/content/27/2/965.abstract English
spellingShingle Tri Handayani,
Syed Alwi, Sharifah Sakinah
Nallappan, Meenakshii
Lope Pihie, Azimahtol Hawariah
Regulation of p53-, Bcl-2- and Caspase-dependent Signaling Pathway in Xanthorrhizol-induced Apoptosis of HepG2 Hepatoma Cells
title Regulation of p53-, Bcl-2- and Caspase-dependent Signaling Pathway in Xanthorrhizol-induced Apoptosis of HepG2 Hepatoma Cells
title_full Regulation of p53-, Bcl-2- and Caspase-dependent Signaling Pathway in Xanthorrhizol-induced Apoptosis of HepG2 Hepatoma Cells
title_fullStr Regulation of p53-, Bcl-2- and Caspase-dependent Signaling Pathway in Xanthorrhizol-induced Apoptosis of HepG2 Hepatoma Cells
title_full_unstemmed Regulation of p53-, Bcl-2- and Caspase-dependent Signaling Pathway in Xanthorrhizol-induced Apoptosis of HepG2 Hepatoma Cells
title_short Regulation of p53-, Bcl-2- and Caspase-dependent Signaling Pathway in Xanthorrhizol-induced Apoptosis of HepG2 Hepatoma Cells
title_sort regulation of p53-, bcl-2- and caspase-dependent signaling pathway in xanthorrhizol-induced apoptosis of hepg2 hepatoma cells
url http://psasir.upm.edu.my/id/eprint/7266/
http://psasir.upm.edu.my/id/eprint/7266/
http://psasir.upm.edu.my/id/eprint/7266/1/Regulation%20of%20p53.pdf