据韩联社22日报道，韩国科学家今天表示，他们发现了一种可以用来抑制人体内癌细胞生长或完全杀死癌细胞的基因。
首尔大学郑用瑾教授领导的研究小组的这项发现揭示，从线粒体膜间释放的腺苷酸激酶2(AK2)基因可以导致错误生成的细胞自行毁灭。
几乎所有活着的细胞中都有线粒体，它是“细胞发电站”，能够产生维持生命所必需的化学能量。
普通细胞有一定的生命周期。存活一段时间后，这些细胞就会死亡，其位置由新细胞顶替。癌细胞不遵循这一模式，它们会一直生长，直到威胁宿主的生命。
这项成果刊登在最新一期的《自然-细胞生物学》杂志上。研究报告说，肝癌患者体内显然缺少AK2基因。
郑用瑾说：“详细检查显示，如果AK2基因弱或不起作用，癌细胞就会成倍增加。”他还说，如果AK2基因“复活”，患者接受抗癌治疗的效果就更好。
郑用瑾说，如果科学家们能够找到一种方法控制AK2基因的释放，那么他们就能从癌症初期开始遏制癌细胞生长，或更便于癌症患者的治疗。(新华网)
原始出处:
Published online: 21 October 2007; | doi:10.1038/ncb1650
AK2 activates a novel apoptotic pathway through formation of a complex with FADD and caspase-10
Ho-June Lee1, 2, Jong-Ok Pyo2, Yumin Oh2, Hyo-Jin Kim2, Se-hoon Hong2, Young-Jun Jeon2, Hyunjoo Kim2, Dong-Hyung Cho1, Ha-Na Woo1, Sungmin Song2, Jung-Hyun Nam1, Hyo Joon Kim3, Key-Sun Kim4 & Yong-Keun Jung1, 2
1 Department of Life Science, Gwangju Institute of Science and Technology, 261 Cheomdan-gwagiro, Buk-gu, Gwangju 500–712, Korea.
2 School of Biological Science/Bio-Max Institute, Seoul National University, 599 Gwanangno, Gwanak-gu, Seoul 151–742, Korea.
3 Division of Moecular and Life Sciences, Hanyang University, 1271 Sa-1 dong, Sangnok-gu, Ansan, Gyeonggi 426-791, Korea.
4 Center for Neural Science, Korea Institute of Science and Technology, 39-1 Hawolgok-dong, Seongbuk-gu, Seoul 136–791, Korea.
Correspondence should be addressed to Yong-Keun Jung ykjung@snu.ac.kr
Mitochondrial proteins function as essential regulators in apoptosis. Here, we show that mitochondrial adenylate kinase 2 (AK2) mediates mitochondrial apoptosis through the formation of an AK2–FADD–caspase-10 (AFAC10) complex. Downregulation of AK2 attenuates etoposide- or staurosporine-induced apoptosis in human cells, but not that induced by tumour-necrosis-factor-related apoptosis-inducing ligand (TRAIL) or Fas ligand (FasL). During intrinsic apoptosis, AK2 translocates to the cytoplasm, whereas this event is diminished in Apaf-1 knockdown cells and prevented by bcl-2 or Bcl-XL. Addition of purified AK2 protein to cell extracts first induces activation of caspase-10 via FADD and subsequently caspase-3 activation, but does not affect caspase-8. AFAC10 complexes are detected in cells undergoing intrinsic cell death and AK2 promotes the association of caspase-10 with FADD. In contrast, AFAC10 complexes are not detected in several etoposide-resistant human tumour cell lines. Taken together, these results suggest that, acting in concert with FADD and caspase-10, AK2 mediates a novel intrinsic apoptotic pathway that may be involved in tumorigenesis.
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