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Ethanol extract of Dunaliella salina induces cell cycle arrest and apoptosis in A549 human non-small cell lung cancer cells

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Author(s): Sheu, MJ (Sheu, Ming-Jyh); Huang, GJ (Huang, Guan-Jhong); Wu, CH (Wu, Chieh-Hsi); Chen, JS (Chen, Jwo-Sheng); Chang, HY (Chang, Heng-Yuan); Chang, SJ (Chang, Shu-Jen); Chung, JG (Chung, Jing-Gung)

Title: Ethanol extract of Dunaliella salina induces cell cycle arrest and apoptosis in A549 human non-small cell lung cancer cells

Source: IN VIVO, 22 (3): 369-378 MAY-JUN 2008 Language: English

Document Type: Article

Author Keywords: Dunaliella salina; beta-carotene; apoptosis; A549; p53; NSCLS

KeyWords Plus: 9-CIS BETA-CAROTENE; ANTIOXIDANT ACTIVITY; IN-VIVO; ASCORBIC- ACID; VITAMIN-E; ACTIVATION; EXPRESSION; BARDAWIL; ALGAE; RATS

Abstract: The ethanol extract of Dunaliella salina (EDS) on proliferation and apoptosis in the A549 human lung cancer cell line and their associated protein expressions were investigated.

After 24 and 48 h treatment, MTT assay showed that 25 mu g/ml of EDS significantly reduced A549 cell proliferation by 25.2% (p<0.05) and 48.3% (p<0.01), respectively. To explore its molecular mechanisms in regulating cell proliferation, we first showed that EDS markedly reduced A549 proliferation via inhibition of BrdU incorporation at 25 mu g/ml by 65.8%

(p<0.001). By cytometric analysis, EDS was found to induce apoptosis and cell cycle arrest in the G0/G1 phase. In the DNA gel electrophoresis assay, EDS (25, 50 and 100 mu g/ml) induced significant apoptosis at 48 h. Annexin V/Propodium iodide double staining

demonstrated that administration of EDS (25 mu g/ml) in 12, 24 and 48 h induces apoptosis of 27.7%, 30.7%, and 38.7%. Western blotting assay demonstrated that EDS significantly increased the expression of cyclin-dependent kinase (CDK) inhibitors p53 and p21 and death- receptor proteins Fas and FasL. Bax expression was also elevated by treatment with EDS.

Our data suggested that EDS could influence the antiproliferative effects and induce cell cycle G0/G1 arrest and apoptosis of A549 lung cancer cells.

Addresses: [Chung, Jing-Gung] China Med Univ, Coll Med, Dept Biol Sci & Technol, Taichung 404, Taiwan; [Sheu, Ming-Jyh] China Med Univ, Dept Physiol, Taichung 404, Taiwan; [Chen, Jwo-Sheng] China Med Univ, Dept Sports Med, Taichung 404, Taiwan;

[Huang, Guan-Jhong; Chang, Heng-Yuan] China Med Univ, Inst Chinese Pharmaceut Sci, Taichung 404, Taiwan; [Sheu, Ming-Jyh; Wu, Chieh-Hsi; Chang, Shu-Jen] China Med Univ, Sch Pharm, Taichung 404, Taiwan; [Chung, Jing-Gung] Asia Univ, Dept Biotechnol, Wufeng, Taichung County, Taiwan

Reprint Address: Chung, JG, China Med Univ, Coll Med, Dept Biol Sci & Technol, 91,Hsueh Shih Rd, Taichung 404, Taiwan.

E-mail Address: [email protected]

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Cited Reference Count: 35 Times Cited: 1

Publisher: INT INST ANTICANCER RESEARCH

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Publisher Address: EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22, ATHENS 19014, GREECE

ISSN: 0258-851X

29-char Source Abbrev.: IN VIVO ISO Source Abbrev.: In Vivo Source Item Page Count: 10

Subject Category: Medicine, Research & Experimental ISI Document Delivery No.: 312XG

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