青青天涯草
暫缺
癌細胞的快速分裂和生長，這個過程需要大量能量作為支撐，英國研究人員日前發表報告說，他們找到了一種能夠限製癌細胞能量來源的方法，可以通過這種方式“餓死”癌細胞幫助治療癌症。
新一期《自然·細胞生物學》報告說，癌細胞通常依靠分解葡萄糖來獲取能量，如果體內的葡萄糖含量不足則轉向別的能量來源，研究人員發現一種名為NF-kB*的蛋白質控製著其能量供應方式的轉換，如果抑製這種蛋白質的功能，癌細胞就不能按需轉換能量供應方式，會進入能量供應不足的狀態甚至“餓死”。
研究人員在實驗室中用腸癌細胞進行了實驗，結果顯示可以通過這種限製能量供應的方式來殺死癌細胞。此外，如果在抑製蛋白質NF-kB的功能的同時，使用一種已有的糖尿病藥物二甲雙胍，則“餓死”癌細胞的效率會大大提高。
這是首次揭示NF-kB具有調節細胞能量來源的功能，以前雖然也知道它在癌症中發揮著某種作用，但具體機理不是很清楚，因此與之相關的癌症治療方式效果也不太理想。本次研究還發現可以將它和二甲雙胍聯合使用，有望在此基礎上研發出更有效的癌症治療方式。
*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.
**二甲雙胍: 雙胍類降糖藥，口服。適用於單用飲食和運動治療不能獲良好控製的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
哈哈，我想改變一下風格，雨痕卻變換了風貌，真是不約而同啊！
兜兄的博文都忘不了研究醫學課題啊~~真是個學究~~：）