Pallavi Rani, Giorgio Marco, Pelicci Pier G
European Institute of Oncology Milan, Italy.
Front Physiol. 2012 Aug 9;3:318. doi: 10.3389/fphys.2012.00318. eCollection 2012.
Over the last several years, new evidence has kept pouring in about the remarkable effect of caloric restriction (CR) on the conspicuous bedfellows- aging and cancer. Through the use of various animal models, it is now well established that by reducing calorie intake one can not only increase life span but, also, lower the risk of various age related diseases such as cancer. Cancer cells are believed to be more dependent on glycolysis for their energy requirements than normal cells and, therefore, can be easily targeted by alteration in the energy-metabolic pathways, a hallmark of CR. Apart from inhibiting the growth of transplantable tumors, CR has been also shown to inhibit the development of spontaneous, radiation, and chemically induced tumors. The question regarding the potentiality of the anti-tumor effect of CR in humans has been in part answered by the resistance of a cohort of women, who had suffered from anorexia in their early life, to breast cancer. However, human research on the beneficial effect of CR is still at an early stage and needs further validation. Though the complete mechanism of the anti-tumor effect of CR is far from clear, the plausible involvement of nutrient sensing pathways or IGF-1 pathways proposed for its anti-aging action cannot be overruled. In fact, cancer cell lines, mutant for proteins involved in IGF-1 pathways, failed to respond to CR. In addition, CR decreases the levels of many growth factors, anabolic hormones, inflammatory cytokines, and oxidative markers that are deregulated in several cancers. In this review, we discuss the anti-tumor effect of CR, describing experiments done in vitro in tumor models and in vivo in mouse models in which the tumor was induced by means of radiation or chemical exposure, expressing oncogenes or deleting tumor suppression genes. We also discuss the proposed mechanisms of CR anti-tumor action. Lastly, we argue the necessity of gene expression studies in cancerous versus normal cells upon CR.
在过去几年里,关于热量限制(CR)对衰老和癌症这两个明显相关因素的显著影响,新证据不断涌现。通过使用各种动物模型,现在已经明确,通过减少卡路里摄入量,不仅可以延长寿命,还能降低患各种与年龄相关疾病(如癌症)的风险。据信,癌细胞比正常细胞更依赖糖酵解来满足其能量需求,因此,能量代谢途径的改变(CR的一个标志)很容易靶向癌细胞。除了抑制可移植肿瘤的生长外,CR还被证明能抑制自发、辐射和化学诱导肿瘤的发展。一组早年患有厌食症的女性对乳腺癌具有抵抗力,这在一定程度上回答了CR对人类抗肿瘤作用潜力的问题。然而,关于CR有益效果的人体研究仍处于早期阶段,需要进一步验证。尽管CR抗肿瘤作用的完整机制尚不清楚,但不能排除其抗衰老作用中所提出的营养感应途径或IGF-1途径的合理参与。事实上,IGF-1途径中相关蛋白质发生突变的癌细胞系对CR没有反应。此外,CR降低了许多在几种癌症中失调的生长因子、合成代谢激素、炎性细胞因子和氧化标志物的水平。在这篇综述中,我们讨论了CR的抗肿瘤作用,描述了在肿瘤模型中体外进行的实验以及在通过辐射或化学暴露诱导肿瘤、表达癌基因或缺失肿瘤抑制基因的小鼠模型中体内进行的实验。我们还讨论了CR抗肿瘤作用的 proposed机制。最后,我们论证了在CR作用下对癌细胞与正常细胞进行基因表达研究的必要性。 (注:“proposed”未翻译,可能是原文有误,推测可能是“proposed”,暂按此处理)