Molecular cell：关键突变导致癌细胞代谢“重连”促进药物抵抗

2015-07-07 佚名生物谷

                                                       &nbs

最近，来自艾默里大学的科学家发现在许多黑色素瘤中存在一个重要基因突变能够使癌细胞的代谢重新连线，使癌细胞的生长依赖于一种参与酮体生成的催化酶，这一发现为解决黑色素瘤细胞对靶向药物的抵抗，开发新的替代药物提供了深入见解，同时也部分解释了为什么这一突变在黑色素瘤细胞中频发。近日，相关研究结果发表在国际学术期刊molecular cell。

B-raf基因发生V600E突变在黑色素瘤细胞中非常常见，这一突变能够促进癌细胞生长，除了在黑色素瘤中存在，在一些结肠癌和甲状腺癌病例中也发现存在B-raf V600E突变。目前已经开发出一些针对B-raf V600E基因突变的靶向药物，但在临床实验中发现，在癌症得到明显改善之后，携带V600E基因突变的癌细胞都不可避免地产生药物抗性。

在这项研究中，研究人员发现B-raf V600E基因突变能够刺激癌细胞产生更多的HMG-CoA裂解酶，携带V600E突变的黑色素瘤细胞生长非常依赖于该酶，而其他的黑色素瘤细胞则不会。HMG-CoA裂解酶是酮体生成途径中一个重要酶，能够帮助机体在血糖水平较低时降解脂肪酸以获得能量。酮体生成途径能够受到低糖，高脂饮食刺激激活，通常发生于肝脏，但B-raf V600E基因突变启动了癌细胞中的酮体生成，以维持癌细胞生长存活。除此之外，研究人员还发现酮体生成途径的重要产物乙酰乙酸能够刺激携带B-raf V600E基因突变的癌细胞继续增殖。

总得来说，这项研究证明B-raf V600E基因突变能够使黑色素瘤细胞中的代谢途径重新连线，增强癌细胞对酮体生成途径的依赖性，这一发现对于解决黑色素瘤细胞对靶向药物的抵抗，开发新的替代药物具有重要意义。

原始出处：

Hee-Bum Kang14, Jun Fan14, Ruiting Lin14, Shannon Elf, Quanjiang Ji, Liang Zhao, Lingtao Jin, Jae Ho Seo, Changliang Shan, Jack L. Arbiser, Cynthia Cohen, Daniel Brat, Henry M. Miziorko, Eunhee Kim, Omar Abdel-Wahab, Taha Merghoub, Stefan Fröhling, Claudia Scholl, Pablo Tamayo, David A. Barbie, Lu Zhou, Brian P. Pollack, Kevin Fisher, Ragini R. Kudchadkar, David H. Lawson, Gabriel Sica, Michael Rossi, Sagar Lonial, Hanna J. Khoury, Fadlo R. Khuri, Benjamin H. Lee, Titus J. Boggon, Chuan He, Sumin Kangcorrespondenceemail, Jing Chen.Metabolic Rewiring by Oncogenic BRAF V600E Links Ketogenesis Pathway to BRAF-MEK1 Signaling.Molecular Cell.July 2, 2015.

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2015-07-16 zhaozhouchifen

#Cell#

23 0
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2015-11-15 智智灵药

#CEL#

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2015-07-08 yxch36

#癌细胞#

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2015-07-08 jambiya

#致癌#

29 0
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2015-07-08 yangshch

#细胞代谢#

24 0
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