癌细胞的快速分裂和生长，这个过程需要大量能量作为支撑，英国研究人员日前发表报告说，他们找到了一种能够限制癌细胞能量来源的方法，可以通过这种方式“饿死”癌细胞帮助治疗癌症。

新一期《自然·细胞生物学》报告说，癌细胞通常依靠分解葡萄糖来获取能量，如果体内的葡萄糖含量不足则转向别的能量来源，研究人员发现一种名为NF-kB*的蛋白质控制着其能量供应方式的转换，如果抑制这种蛋白质的功能，癌细胞就不能按需转换能量供应方式，会进入能量供应不足的状态甚至“饿死”。

研究人员在实验室中用肠癌细胞进行了实验，结果显示可以通过这种限制能量供应的方式来杀死癌细胞。此外，如果在抑制蛋白质NF-kB的功能的同时，使用一种已有的糖尿病药物二甲双胍，则“饿死”癌细胞的效率会大大提高。

这是首次揭示NF-kB具有调节细胞能量来源的功能，以前虽然也知道它在癌症中发挥着某种作用，但具体机理不是很清楚，因此与之相关的癌症治疗方式效果也不太理想。本次研究还发现可以将它和二甲双胍联合使用，有望在此基础上研发出更有效的癌症治疗方式。

*NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex that controls the transcription of DNA, involved in 1) cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens and 2) plays a key role in regulating the immune response to infection . Incorrect regulation of NF-κB has been linked to cancer, inflammatory and autoimmune diseases, septic shock, viral infection, and improper immune development. NF-κB has also been implicated in processes of synaptic plasticity and memory.
 **二甲双胍: 双胍类降糖药，口服。适用于单用饮食和运动治疗不能获良好控制的2型糖尿病患者。

Original abstract: Cell proliferation is a metabolically demanding process. It requires active reprogramming of cellular bioenergetic pathways towards glucose metabolism to support anabolic growth. NF-κB/Rel transcription factors coordinate many of the signals that drive proliferation during immunity, inflammation and oncogenesis, but whether NF-κB regulates the metabolic reprogramming required for cell division during these processes is unknown. Here, we report that NF-κB organizes energy metabolism networks by controlling the balance between the utilization of glycolysis and mitochondrial respiration. NF-κB inhibition causes cellular reprogramming to aerobic glycolysis under basal conditions and induces necrosis on glucose starvation. The metabolic reorganization that results from NF-κB inhibition overcomes the requirement for tumour suppressor mutation in oncogenic transformation and impairs metabolic adaptation in cancer in vivo. This NF-κB-dependent metabolic pathway involves stimulation of oxidative phosphorylation through upregulation of mitochondrial synthesis of cytochrome c oxidase 2 (SCO2). Our findings identify NF-κB as a physiological regulator of mitochondrial respiration and establish a role for NF-κB in metabolic adaptation in normal cells and cancer. Mauro C and et al.,Nature Cell Biology, 8/28/2011