Nature:一氨基酸可显著削弱癌细胞增殖能力

2013-01-09 Nature 互联网 何嫱

自英国Beatson癌症研究所的研究人员在一项新研究中证实,夺去癌细胞的一种关键氨基酸可显着削弱它们的生长和增殖能力。这一研究发现在线发表在12月16日的《自然》(Nature)杂志上。 Beatson癌症研究所的科学家们研究了当缺乏丝氨酸时癌细胞能够生存并继续生长的机制。细胞通常能够自己生成丝氨酸,然而研究小组发现缺乏p53蛋白的细胞(至少一半的癌症存在这种缺陷)则无法适应这一转变,因此其生长


自英国Beatson癌症研究所的研究人员在一项新研究中证实,夺去癌细胞的一种关键氨基酸可显着削弱它们的生长和增殖能力。这一研究发现在线发表在12月16日的《自然》(Nature)杂志上。

Beatson癌症研究所的科学家们研究了当缺乏丝氨酸时癌细胞能够生存并继续生长的机制。细胞通常能够自己生成丝氨酸,然而研究小组发现缺乏p53蛋白的细胞(至少一半的癌症存在这种缺陷)则无法适应这一转变,因此其生长速度大为放缓。

p53蛋白最早是被英国癌症研究院的科学家们所发现,由于它能够停止受损细胞生长,激活DNA修复或启动细胞死亡,通常被称为是“基因组的卫士”。

研究结果表明,通过靶向癌细胞生成生长所需能量及构件的途径,可以开发出治疗癌症的新方法。

英国Beatson癌症研究所首席研究员Oliver Maddocks博士说:“我们知道p53蛋白可以阻止癌细胞生长,但我们也越来越认识到p53是一种具有‘分裂人格’的基因。当细胞缺乏关键营养时,p53会帮助它们适应,并有可能帮助癌细胞生存。“

“了解细胞代谢与p53之间的相互作用,或许有助于我们确定治疗癌症的新途径。减少癌细胞的丝氨酸利用率,尤其是缺失p53的癌细胞,是一种有前景的新概念,然而确定这是否能对患者起作用还有一个漫长的过程。”

癌细胞摄取大量的丝氨酸,以它作为基本构件快速生长并生成新细胞。本研究是建立在Beatson研究所过往的研究工作基础上:癌细胞中丝氨酸的水平控制了能量生成的一个关键步骤。

英国癌症研究院的首席科学家Nic Jones教授说:“这项工作表明,在英国癌症研究中心的科学家们发现p53的30年之后,我们仍然可以了解到更多p53在癌症中发挥作用的信息。”

“了解癌细胞能够生成额外能量和分子构件快速生长的机制,正变成一个重要的研究领域。扰乱细胞代谢有可能导致全新的治疗癌症的药物库,英国癌症研究院处于本研究的前沿。”

doi:10.1038/nature11743
PMC:
PMID:

Serine starvation induces stress and p53-dependent metabolic remodelling in cancer cells

Oliver D. K. Maddocks Celia R. Berkers Susan M. Mason Liang Zheng Karen Blyth Eyal Gottlieb Karen H. Vousden

Cancer cells acquire distinct metabolic adaptations to survive stress associated with tumour growth and to satisfy the anabolic demands of proliferation. The tumour suppressor protein p53 (also known as TP53) influences a range of cellular metabolic processes, including glycolysis1, 2, oxidative phosphorylation3, glutaminolysis4, 5 and anti-oxidant response6. In contrast to its role in promoting apoptosis during DNA-damaging stress, p53 can promote cell survival during metabolic stress7, a function that may contribute not only to tumour suppression but also to non-cancer-associated functions of p538. Here we show that human cancer cells rapidly use exogenous serine and that serine deprivation triggered activation of the serine synthesis pathway and rapidly suppressed aerobic glycolysis, resulting in an increased flux to the tricarboxylic acid cycle. Transient p53-p21 (also known as CDKN1A) activation and cell-cycle arrest promoted cell survival by efficiently channelling depleted serine stores to glutathione synthesis, thus preserving cellular anti-oxidant capacity. Cells lacking p53 failed to complete the response to serine depletion, resulting in oxidative stress, reduced viability and severely impaired proliferation. The role of p53 in supporting cancer cell proliferation under serine starvation was translated to an in vivo model, indicating that serine depletion has a potential role in the treatment of p53-deficient tumours.

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    2013-09-28 liye789132251
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    2013-01-11 yxch36
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来自中山大学癌症中心、范德堡大学医学院的研究人员确定了三个与大肠癌相关的新遗传“热点”。研究发现在线发表在12月23日的《自然遗传学》(Nature Genetic)杂志上,从而为我们提供了关于大肠癌生物学的新认识,有可能指出了该疾病新的治疗靶点。 领导这一研究的是华人科学家郑苇(Wei Zheng)教授,其现任范德堡大学Ingram癌症研究中心教授、分子流行病研究室主任,亦为美国NCI基金项目