Pomolic acid induces apoptosis in SK-OV-3 human ovarian adenocarcinoma cells through the mitochondrial-mediated intrinsic and death receptor-induced extrinsic pathways
The cytotoxic effect of pomolic acid (PA), a pentacyclic triterpene isolated from flowers of Osmanthus fragrans var. aurantiacus Makino, was investigated in SK-OV-3 human ovarian adenocarcinoma cells. PA dose-dependently inhibited the viability of SK-OV-3 cells. PA-induced apoptosis was further char...
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Published in | Oncology letters Vol. 5; no. 1; pp. 386 - 390 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Greece
D.A. Spandidos
01.01.2013
Spandidos Publications UK Ltd |
Subjects | |
Online Access | Get full text |
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Summary: | The cytotoxic effect of pomolic acid (PA), a pentacyclic triterpene isolated from flowers of Osmanthus fragrans var. aurantiacus Makino, was investigated in SK-OV-3 human ovarian adenocarcinoma cells. PA dose-dependently inhibited the viability of SK-OV-3 cells. PA-induced apoptosis was further characterized by detection of cell surface annexin V and sub-G1 apoptotic cell populations. The number of cells immunostained with annexin V-fluorescein isothiocyanate (FITC) increased following treatment with PA. The sub-G1 cell populations also increased in PA-treated SK-OV-3 cells. PA induced the activation of caspase-8, -9 and -3, critical mediators of apoptosis signaling. PA decreased the mitochondrial transmembrane potential (ΔΨm), resulting in the activation of caspase-9. In addition, PA increased the expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis signaling-related death receptor 5 (DR5), mediating caspase-8-involved extrinsic pathway. Taken together, our results indicate that PA induces apoptosis in SK-OV-3 cells, which is mediated by the mitochondrial-mediated intrinsic and death receptor-induced extrinsic pathways. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Contributed equally |
ISSN: | 1792-1074 1792-1082 |
DOI: | 10.3892/ol.2012.985 |