Cheah, S. C; Appleton, D. R.; Lee, S. T.; Lam, M. L.; Hadi, A.H.A; Mustafa, M. R. (2011) Panduratin a inhibits the growth of A549 Cells through induction of apoptosis and inhibition of NF-KappaB translocation. Molecules, 16 (3). pp. 2583-2598.
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In the present study we investigated the effects of panduratin A, isolated from Boesenbergia rotunda, on proliferation and apoptosis in A549 human non-small cell lung cancer cells. Cell proliferation and induction of apoptosis was determined by the real-time cellular analyzer (RTCA), MTT assay and High Content Screening (HCS). The RTCA assay indicated that panduratin A exhibited cytotoxicity, with an IC50 value of 4.4 µg/mL 10.8 µM). Panduratin A arrested cancer cells labeled with bromodeoxyuridine (BrdU) and phospho-Histone H3 in the mitotic phase. The cytotoxic effects of panduratin A were found to be accompanied by a dose-dependent induction of apoptosis, as assessed by DNA condensation, nuclear morphology and intensity, cell permeability, mitochondrial mass/potential, F-actin and cytochrome c. In addition, treatment with an apoptosis-inducing concentration of panduratin A resulted in significant inhibition of Nuclear Factor-kappa Beta (NF-κB) translocation from cytoplasm to nuclei activated by tumor necrosis factoralpha (TNF-α), as illustrated by the HCS assay. Our study provides evidence for cell growth inhibition and induction of apoptosis by panduratin A in the A549 cell line,suggesting its therapeutic potential as an NF-κB inhibitor.
|Journal or Publication Title:||Molecules|
|Additional Information:||Centre of Natural Products & Drug Discovery (CENAR), Department of Pharmacology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia; E-Mails: firstname.lastname@example.org (D.R.A.); email@example.com (S.T.L.);|
|Uncontrolled Keywords:||Panduratin A, Apoptosis, High Content Screening, Real-time Cellular Analyzer, NF-κB|
|Subjects:||Q Science > QD Chemistry|
|Depositing User:||Ms Haslinda Lahuddin|
|Date Deposited:||17 Jan 2012 14:26|
|Last Modified:||17 Jan 2012 14:26|
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