Antiproliferative and Proapoptotic Effects of Labisia pumila Ethanol Extract and Its Active Fraction in Human Melanoma HM3KO Cells
Autor: | Azimahtol Hawariah Lope Pihie, Fezah Othman, Zainul Amiruddin Zakaria |
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Jazyk: | angličtina |
Rok vydání: | 2012 |
Předmět: |
Ethanol
biology medicine.diagnostic_test Article Subject business.industry Cell growth Labisia pumila lcsh:Other systems of medicine Cell cycle Pharmacology biology.organism_classification lcsh:RZ201-999 Molecular biology In vitro Flow cytometry chemistry.chemical_compound Complementary and alternative medicine chemistry Apoptosis Medicine Cytotoxic T cell business Research Article |
Zdroj: | Evidence-Based Complementary and Alternative Medicine, Vol 2012 (2012) Evidence-based Complementary and Alternative Medicine : eCAM |
ISSN: | 1741-4288 |
Popis: | The present study was to determine the anticancer potential ofLabisia pumilainin vitromodels. Results from the study revealed that ethanol extract ofL. pumilawas more cytotoxic against HM3KO cells while having reduced effects on nonmalignant cells as compared to aqueous and hexane extracts. Thus, ethanol extract was selected to be further separated by using the bioassay-guided fractionation method to give an active fraction, SF2Lp. Results obtained from the flow cytometry analysis showed that SF2Lp was able to arrest the HM3KO cell cycle at the G1 phase, while morphological findings from AO-EB nuclear staining assays along with the Apoptotic Index confirmed the induction of apoptosis by SF2Lp in HM3KO cells. Results from the mechanistic study further revealed that SF2Lp treatment was able to concurrently increase the expression level of p53 and pro-apoptotic protein Bax and also reduce the expression level of anti-apoptotic protein BCl-2 in HM3KO cells, directly contributing to the increase in Bax/Bcl-2 ratio. These findings, therefore, suggested thatL. pumilawas able to inhibit HM3KO cell growth possibly by arresting the cell cycle at G1 phase and inducing apoptosis in HM3KO cells via the up- and down-regulation of Bax/Bcl-2 protein, mediated through a p53-dependent pathway. |
Databáze: | OpenAIRE |
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