通过RNA-Seq探索omega-3多不饱和脂肪酸抑制前列腺肿瘤的生长机制
首发时间:2018-03-02
摘要:为探究omega-3多不饱和脂肪酸(EPA、DHA)对人前列腺肿瘤体内的作用及其调控机制,本实验采利用先天性免疫缺陷的裸鼠构建LNCaP细胞移植瘤模型,通过EPA、DHA、LA的膳食补充,观察其对前列腺肿瘤体内的作用效果,并通过转录组高通量测序的生物信息学手段,对其作用机理进行初探。动物实验结果表明在小鼠体内omega-3多不饱和脂肪酸可以抑制前列腺肿瘤的生长,尤其是EPA。转录组高通量测序结果中,分别找出EPA、DHA组与N6组肿瘤组织的差异表达基因,发现EPA的作用与DHA的作用机理不同。本研究后续对EPA和N6组的显著差异基因进行GO富集和KEGG pathway富集发现,EPA多作用于细胞与外基质,且与TGF-beta信号通路、类固醇生物合成以及B细胞受体信号相关。因此,本研究为前列腺癌患者更加准确合理的地膳食补充omega-3多不饱和脂肪酸提供理论依据。
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The effect of omega-3 PUFA on human prostate cancer by transcriptomics
Abstract:In order to investigate the effects of omega-3 polyunsaturated fatty acids (EPA/DHA) on human prostate cancer in vivo, LNCaP CDX model was established with dietary supplement of EPA, DHA and LA. The results showed that omega-3 PUFA was able to inhibit the growth of prostate tumor according to the tumor size and weight, especially EPA. We futher studied its mechanism by RNA-Seq. As a basic on the clean data, we have chosen the differentially expressed genes between EPA, DHA and N6. We found that the mechanism of inhibitory effects exerted by EPA was different from that by DHA. Further analyses by GO enrichment and KEGG pathway enrichment, we found that EPA mostly acted on cell surface and extracellular matrix. And EPA could trigger a series of signaling pathway, like TGF-beta signaling pathway, steroid hormone biosynthesis, B cell receptor signaling pathway and so on. These results provides a rational basis for patients with prostate cancer to dietary supplement with omega-3 PUFA.
Keywords: RNA-Seq EPA prostate tumor CDX model
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通过RNA-Seq探索omega-3多不饱和脂肪酸抑制前列腺肿瘤的生长机制
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