Asbestos Information Legal Mesothelioma Clinical: Fwd: Action of resveratrol alone or in combination with roscovitine, a CDK inhibitor, on cell cycle progression in human HL-60 leukemia cells.

Saturday, September 13, 2008

Fwd: Action of resveratrol alone or in combination with roscovitine, a CDK inhibitor, on cell cycle progression in human HL-60 leukemia cells.

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From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Tue, Sep 2, 2008 at 8:26 PM
Subject: Action of resveratrol alone or in combination with roscovitine, a CDK inhibitor, on cell cycle progression in human HL-60 leukemia cells.
To: mesothelioma77@gmail.com

[1]Biochem Pharmacol. 2008 Aug 12;
Komina O, Węsierska-Gądek J

Results of a number of epidemiological and experimental studies indicate that polyphenols (e.g. resveratrol (RES), epicatechins etc.), antioxidant agents and abundant micronutrients in our food could have strong anti-mitotic as well as pro-apoptotic effects. In this study we raised the question whether roscovitine (ROSC), an inhibitor of cyclin-dependent kinases (CDKs) with increased selectivity towards CDK2, could be able to affect human leukemia HL-60 cells in which the p53 gene is inactivated and whether ROSC-induced effects could be additionally modulated by compounds of natural origin, especially by polyphenols e.g. RES. Exposure of HL-60 cells to ROSC for 24h inhibited their proliferation. Flow cytometric analyses revealed that unlike MCF-7 cells, HL-60 cells were arrested in G(1) upon ROSC treatment. Furthermore, ROSC also induced apoptosis in HL-60 cells. After treatment with 40muM ROSC for 24h the frequency of hypoploid cells representing cells undergoing apoptosis reached approximately 50%. In the next step the action of RES alone or in combination with ROSC was examined. Interestingly, synergistic effects were observed after combined treatment for 24h and sequential post-incubation for 48h in the presence of RES. Such combined treatment resulted in a marked reduction of the frequency of the S- and G(2)/M-phase cells and simultaneously increased the G(1) cell population up to 80% at a fourfold lower ROSC dose. Further analyses revealed that the combined treatment strongly activated caspase-3. These results clearly evidence that RES strongly potentiates ROSC-induced apoptosis.

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Source: http://www.hubmed.org/display.cgi?uids=18761329
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