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首页> 外文期刊>Journal of Cellular Physiology >Regulation of prostate cancer cell division by glucose.
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Regulation of prostate cancer cell division by glucose.

机译：调节前列腺癌的细胞分裂葡萄糖。

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Previous studies have shown that rapid cell proliferation is associated with elevated glucose consumption. However, those studies did not establish whether glucose is required for prostate cancer cell proliferation or define the molecular mechanisms by which glucose regulates cell division. We addressed these issues by studying two metastatic human prostate cancer cell lines: DU145, which is androgen independent and highly proliferative; and LNCaP, which is androgen dependent and relatively slow growing. We found that proliferation of DU145 cells was significantly inhibited by reduction of glucose in the medium to 0.5 g/L, which is half the physiologic concentration, whereas LNCaP cells grew at control rates even in the presence of only 0.05 g/L glucose. Glucose deprivation of DU145 cells caused a 90% reduction in DNA synthesis; a 10-20-fold reduction in cyclins D and E and CDK4 levels; and cell cycle arrest in G0-G1. However, glucose deprivation did not cause global inhibition of protein synthesis, since mutant p53 levels increased in glucose-deprived DU145 cells. This observed increase in mutant p53 levels was not associated with a rise in p21 levels. Glucose deprivation of DU145 cells also led to apparent dephosphorylation of mutant retinoblastoma (RB) protein. We conclude that: 1) high levels of glucose consumption are required for rapid proliferation of androgen-independent prostate cancer cells, 2) glucose may not be required for slow growth of androgen-dependent prostate cancer cells, and 3) glucose promotes passage of cells through early G1 by increasing the expression of several key cell cycle regulatory proteins that normally inhibit RB function.
机译：之前的研究表明,快速的细胞扩散与血糖升高有关消费。确定是否需要葡萄糖前列腺癌的细胞增殖或定义葡萄糖调节的分子机制细胞分裂。研究两个人类前列腺癌转移细胞系:DU145,雄激素独立和高度增殖;雄激素依赖性和相对缓慢的增长。我们发现DU145细胞扩散显著抑制减少葡萄糖在中0.5 g / L,这是一半生理浓度,而LNCaP细胞增长速度控制甚至在的存在只有0.05 g / L葡萄糖。DU145细胞减少90%的DNA造成的合成;和E和到水平;G0-G1。全球抑制蛋白质合成,因为突变型p53在glucose-deprived水平增加DU145细胞。p21水平没有上升的水平。导致明显的去磷酸化的突变视网膜母细胞瘤(RB)的蛋白质。高水平的葡萄糖消耗是必需的快速androgen-independent扩散前列腺癌细胞,2)葡萄糖可能不是所需androgen-dependent的缓慢增长前列腺癌细胞,3)葡萄糖促进通过细胞通过早期G1增加几个关键的细胞周期的表达通常抑制RB的调控蛋白函数。

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