The role of lipid metabolism in prostate cancer

进行了各种基础研究以阐明脂质对前列腺癌的影响。首先，角鲨烯合成酶，这是甲羟戊酸途径的关键酶进行了评估。我们先前的研究显示，编码角鲨烯合酶的FDFT 1的SNP与前列腺癌的发生风险相关。目前的研究表明，FDFT 1基因表达的下调导致显着抑制肿瘤增殖。此外，FDFT 1基因表达水平与前列腺癌的生物学侵袭性相关。接着，评价他汀类药物对LDL受体的作用。前列腺癌细胞是他汀类药物的靶点。他汀类调节LDL受体表达谱和细胞中的胆固醇含量。这些调节事件与前列腺癌增殖相关。最后，评价二甲双胍的效果。二甲双胍通过下调IGF1受体抑制前列腺癌增殖。

Various basic studies were conducted to elucidate the effect of lipids on prostate cancer. First, squalene synthase, which is the key enzyme in mevalonate pathway is evaluated. Our previous study revealed that the SNP of FDFT1, which encodes squalene synthase, was associated with risk of prostate cancer development. The present study showed that down-regulation of FDFT1 gene expression led to significant inhibition of cancer proliferation. Furthermore, the FDFT1 gene expression levels were correlated with biological aggressiveness of prostate cancer. Next, the effect of statin was evaluated as to LDL receptor. Prostate cancer cells were the target of statin. Statin regulated both LDL receptor expression profiles and cholesterol content in the cell. These regulatory events were relevant to prostate cancer proliferation. Finally, the effect of metformin was evaluated. Metformin inhibit prostate cancer proliferation via down-regulation of IGF1-receptor.