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Investigation of extrinsic and intrinsic apoptosis pathways of new clerodane diterpenoids in human prostate cancer PC-3 cells.

Abstract：

:In our continuing search to discover bioactive compounds from natural products, we isolated six new clerodane diterpenes, caseamembrins A to F, from Casearia membranacea and examined their antiproliferative activities in human hormone-resistant prostate cancer PC-3 cells. All of these compounds displayed effective antiproliferative activity using sulforhodamine B assays and induced cell apoptosis by a terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL)-reaction technique. The data demonstrated that caseamembrin C was the most effective compound among these clerodane diterpenoids. Caseamembrin C induced down-regulation of Bcl-2 and Bcl-xL expression, while up-regulation of proapoptotic protein Mcl-1S (short chain), suggesting that these Bcl-2 family member proteins may play a role on arbitrating the apoptotic cell death. Caseamembrin C also induced the up-regulation of Fas ligand (FasL) expression, cleavage and activation of caspase-8 and caspase-9, Bid cleavage and activation of executor caspase-3. However, z-IETD-FMK (Z-Ile-Glu-Thr-Asp-fluoromethyl ketone, a selective caspase-8 inhibitor) almost completely inhibited caseamembrin C-induced Bid cleavage without any modification of caspase-9 activation, indicating that the extrinsic pathway of FasL/caspase-8/Bid cascade only played a minor role in the apoptotic signaling. Taken together, it is suggested that caseamembrin C-induced apoptosis is predominantly through the activation of intrinsic apoptosis pathways by causing the down-regulation of Bcl-2 and Bcl-xL expression, up-regulation of Mcl-1S protein and activation of caspase-9 and caspase-3.

journal_name

Eur J Pharmacol

journal_title

European journal of pharmacology

authors

Huang DM,Shen YC,Wu C,Huang YT,Kung FL,Teng CM,Guh JH

doi

10.1016/j.ejphar.2004.09.040

keywords:

subject

Has Abstract

pub_date

2004-10-25 00:00:00

pages

17-24

issue

1-3

eissn

0014-2999

issn

1879-0712

pii

S0014-2999(04)01075-1

journal_volume

503

pub_type

杂志文章

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