Yu Chun-Xiao, Zhang Xiao-Qian, Kang Lu-Dong, Zhang Peng-Ju, Chen Wei-Wen, Liu Wen-Wen, Liu Qing-Wei, Zhang Jian-Ye
Department of Biochemistry and Molecular Biology, Shandong University School of Medicine, Jinan, China.
Asian J Androl. 2008 Jul;10(4):625-34. doi: 10.1111/j.1745-7262.2008.00397.x.
To elucidate effects and mechanisms of emodin in prostate cancer cells.
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.
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.
In prostate cancer cell line, LNCaP, emodin inhibites the proliferation by AR and p53-p21 pathways, and induces apoptosis via the mitochondrial pathway.
阐明大黄素对前列腺癌细胞的作用及其机制。
采用MTT法检测大黄素处理的LNCaP细胞和PC-3细胞的活力。大黄素处理后，通过琼脂糖凝胶电泳检测DNA片段化。采用流式细胞术分析凋亡率以及Fas和FasL的表达。通过RT-PCR检测雄激素受体（AR）、前列腺特异性抗原（PSA）、p53、p21、Bcl-2、Bax、半胱天冬酶-3、-8、-9和Fas的mRNA表达水平，通过蛋白质免疫印迹分析检测AR、p53和p21的蛋白质表达水平。
与PC-3细胞不同，大黄素可显著增加LNCaP细胞的凋亡并降低其细胞增殖。随着大黄素浓度的增加，AR和PSA的表达降低，p53和p21的表达增加。同时，大黄素通过上调半胱天冬酶-3和-9以及增加Bax/Bcl-2比值诱导LNCaP细胞凋亡。然而，它不涉及Fas或半胱天冬酶-8蛋白表达的调节。
在前列腺癌细胞系LNCaP中，大黄素通过AR和p53-p21途径抑制增殖，并通过线粒体途径诱导凋亡。
