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Abstract

Volume 10, Issue 4 (July 2008) 10, 625–634; 10.1111/j.1745-7262.2008.00397.x

Emodin induces apoptosis in human prostate cancer cell LNCaP

Chun-Xiao Yu, Xiao-Qian Zhang, Lu-Dong Kang, Peng-Ju Zhang, Wei-Wen Chen, Wen-Wen Liu, Qing-Wei Liu and Jian-Ye Zhang

1.Department of Biochemistry and Molecular Biology, Shandong University School of Medicine, Jinan 250012, China
2.Merck Sharp & Dohme, Beijing 100738, China
3.Positron Emission Tomography and Computer Tomography (PET-CT) Center, Shandong Provincial Hospital, Jinan 250021, China

Correspondence: Prof. Jian-Ye Zhang, Department of Biochemistry and Molecular Biology, Shandong University School of Medicine, Jinan 250012, China. E-mail: zhjy@sdu.edu.cn; Dr Qing-Wei Liu, Positron Emission Tomography and Computer Tomography (PET-CT) Center, Shandong Pr

Received 23 May 2007; Accepted 11 January 2008.

Abstract

Aim: To elucidate effects and mechanisms of emodin in prostate cancer cells.

Methods: Viability of emodin-treated LNCaP cells and PC-3 cells was measured by MTT assay. Following emodin treatments, DNA fragmentation was assayed by agarose gel electrophoresis. Apoptosis rate and the expression of Fas and FasL were assayed by flow cytometric analysis. The mRNA expression levels of androgen receptor (AR), prostate-specific antigen (PSA), p53, p21, Bcl-2, Bax, caspase-3, -8, -9 and Fas were detected by RT-PCR, and the protein expression levels of AR, p53 and p21 were detected by Western blot analysis.

Results: In contrast to PC-3, emodin caused a marked increase in apoptosis and a decrease in cell proliferation in LNCaP cells. The expression of AR and PSA was decreased and the expression of p53 and p21 was increased as the emodin concentrations were increased. In the same time, emodin induced apoptosis of LNCaP cells through the upregulation of caspase-3 and -9, as well as the increase of Bax/Bcl-2 ratio. However, it did not involve modulation of Fas or caspase-8 protein expression.

Conclusion: In prostate cancer cell line, LNCaP, emodin inhibites the proliferation by AR and p53-p21 pathways, and induces apoptosis via the mitochondrial pathway.

Keywords: emodin, prostate cancer, LNCaP, PC-3, proliferation, androgen receptor, p53, apoptosis, mitochondrial pathway

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