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首页> 外文期刊>Journal of Cellular Physiology >Mcl-1 targeting could be an intriguing perspective to cure cancer
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Mcl-1 targeting could be an intriguing perspective to cure cancer

机译：mcl1的目标可能是一个有趣的视角治疗癌症

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The Bcl-2 family, which plays important roles in controlling cancer development, is divided into antiapoptotic and proapoptotic members. The change in the balance between these members governs the life and death of the cells. Mcl-1 is an antiapoptotic member of this family and its distribution in normal and cancerous tissues strongly differs from that of Bcl-2. In human cancers, where upregulation of antiapoptotic proteins is common, Mcl-1 expression is regulated independent of Bcl-2 and its inhibition promotes senescence, a major barrier to tumorigenesis. Cancer chemotherapy determines various kinds of responses, such as senescence and autophagy; however, the ideal response to chemotherapy is apoptosis. Mcl-1 is a potent oncogene that is regulated at the transcriptional, posttranscriptional, and posttranslational levels. Mcl-1 is a short-lived protein that, in the NH2 terminal region, contains sites for posttranslational regulation that can lead to proteasomal degradation. The USP9X Mcl-1 deubiquitinase regulates Mcl-1 and the levels of these two proteins are strongly correlated. Mcl-1 has three splicing variants (the antiapoptotic protein Mcl-1L and the proapoptotic proteins Mcl-1S and Mcl-1ES), each contributing toward apoptosis regulation. In cancers responsible for the most deaths in the world, the presence of Mcl-1 is associated with malignant cell growth and evasion of apoptosis. Mcl-1 is also one of the key regulators ofcancer stem cells' self-renewal that contributes to tumor survival. A great number of indirect and selective Mcl-1 inhibitors have been produced and some of these have shown efficacy in several clinical trials. Thus, therapeutic manipulation of Mcl-1 can be a useful strategy to combat cancer.
机译：bcl - 2家族,扮演着重要的角色控制癌症发展,分为凋亡和proapoptotic成员。这些成员之间平衡的变化控制细胞的生与死。一个凋亡这个家庭及其成员分布在正常和癌变组织强烈的不同于bcl - 2。癌症,upregulation凋亡蛋白质是很常见的,mcl1表达式是监管独立的bcl - 2及其抑制促进衰老、肿瘤发生的一个主要障碍。癌症化疗决定各种反应,比如衰老和自噬;然而,理想的化疗反应细胞凋亡。在转录调节,转录后的,转译后的的水平。氨基末端区域,包含网站这会导致转译后的监管蛋白酶体降解。deubiquitinase调节mcl1和的水平这两个蛋白强烈相关。有三个剪接变体(凋亡蛋白质Mcl-1L proapoptotic蛋白质Mcl-1S Mcl-1ES),每个贡献的方向细胞凋亡调控。世界上最死亡的存在mcl1与恶性细胞生长有关和细胞凋亡的逃避。主要监管机构ofcancer干细胞的自我更新,有助于肿瘤的生存。大量的间接和选择性mcl1抑制剂已经产生,其中的一些在几个临床试验显示效果。因此,治疗mcl1可以操纵有用的策略来对抗癌症。

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