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首页> 外文期刊>Lipids in Health Disease >Involvement of apoptotic pathways in docosahexaenoic acid-induced benefit in prostate cancer: Pathway-focused gene expression analysis using RT2 Profile PCR Array System
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Involvement of apoptotic pathways in docosahexaenoic acid-induced benefit in prostate cancer: Pathway-focused gene expression analysis using RT2 Profile PCR Array System

机译：细胞凋亡途径参与二十二碳六烯酸诱导的前列腺癌获益：使用RT2 Profile PCR Array System进行的以途径为中心的基因表达分析

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BackgroundPresent study aimed to better understand the potential apoptotic pathways that involved in docosahexaenoic acid (DHA)-induced apoptosis of prostate cancer cells. MethodsHuman prostate cancer DU145 cells were treated with different concentrations of fish oil, omega-3 PUFA (DHA, and Eicosapentaenoic acid, EPA), or omega-6 PUFA (Arachidonic acid, AA). Cell viability and apoptosis were evaluated by MTT assay and Hoechst staining. Pathway-focused gene expression profiling of DU145 cells was analyzed with the RT2 Profile PCR Array System. The results were verified by real time quantitative polymerase chain reaction (RT-qPCR). ResultsAA exposure showed no obvious effect on viability of DU145 cells. However, exposure with fish oil, EPA, or DHA for 24?h significantly affected cell viability. The growth inhibition of DHA was more pronounced than that of EPA and showed a time-dependent increase. DHA exposure caused typical apoptotic characteristics. Ten genes were more expressed, while 5 genes were less expressed following DHA exposure. RT-qPCR confirmed the time dependent effect of DHA on the expression of these differentially expressed genes. KEGG pathway analysis showed that DHA may induce the apoptosis of cancer cells preferentially through mediating P53, MAPK, TNF, PI3K/AKT, and NF-κB signaling pathways. ConclusionOur study demonstrated the beneficial action of DHA on human prostate carcinoma cell line DU145. The pro-apoptotic effect of DHA on DU145 cells may involve mediation various pathways, especially P53, MAPK, TNF, PI3K/AKT, and NF-κB signaling pathways. Molecular mechanisms of DHA on apoptosis of cancer cells still need to be further clarified.
机译：背景本研究旨在更好地了解二十二碳六烯酸（DHA）诱导的前列腺癌细胞凋亡所涉及的潜在凋亡途径。方法用不同浓度的鱼油，omega-3 PUFA（DHA和二十碳五烯酸，EPA）或omega-6 PUFA（花生四烯酸，AA）处理人前列腺癌DU145细胞。通过MTT测定和Hoechst染色评估细胞活力和凋亡。用RT 2 Profile PCR Array System分析DU145细胞的通路基因表达谱。通过实时定量聚合酶链反应（RT-qPCR）验证了结果。结果AA暴露对DU145细胞活力无明显影响。但是，与鱼油，EPA或DHA接触24小时会显着影响细胞活力。 DHA的生长抑制作用比EPA更为明显，并显示出时间依赖性增加。 DHA暴露引起典型的凋亡特征。 DHA暴露后，十个基因的表达更高，而五个基因的表达则更低。 RT-qPCR证实了DHA对这些差异表达基因的表达具有时间依赖性。 KEGG通路分析表明DHA可通过介导P53，MAPK，TNF，PI3K / AKT和NF-κB信号通路优先诱导癌细胞凋亡。结论我们的研究证明了DHA对人前列腺癌细胞DU145的有益作用。 DHA对DU145细胞的促凋亡作用可能涉及多种途径的介导，尤其是P53，MAPK，TNF，PI3K / AKT和NF-κB信号传导途径。 DHA对癌细胞凋亡的分子机制仍需进一步阐明。

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