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首页> 外文期刊>Biochimica et biophysica acta. Reviews on cancer >Necroptosis: an alternative cell death program defending against cancer
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Necroptosis: an alternative cell death program defending against cancer

机译：坏死病：防御癌症的另一种细胞死亡程序

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摘要

One of the hallmarks of cancer is resistance to programmed cell death, which maintains the survival of cells en route to oncogenic transformation and underlies therapeutic resistance. Recent studies demonstrate that programmed cell death is not confined to caspase-dependent apoptosis, but includes necroptosis, a form of necrotic death governed by Receptor-Interacting Protein 1 (RIP1), RIP3, and Mixed Lineage Kinase Domain-Like (MLKL) protein. Necroptosis serves as a critical cell-killing mechanism in response to severe stress and blocked apoptosis, and can be induced by inflammatory cytokines or chemotherapeutic drugs. Genetic or epigenetic alterations of necroptosis regulators such as RIP3 and cylindromatosis (CYLD), are frequently found in human tumors. Unlike apoptosis, necroptosis elicits a more robust immune response that may function as a defensive mechanism by eliminating tumor-causing mutations and viruses. Furthermore, several classes of anticancer agents currently under clinical development, such as SMAC and BH3 mimetics, can promote necroptosis in addition to apoptosis. A more complete understanding of the interplay among necroptosis, apoptosis, and other cell death modalities is critical for developing new therapeutic strategies to enhance killing of tumor cells. (C) 2016 Elsevier B.V. All rights reserved.
机译：癌症的标志之一是对程序性细胞死亡的抗性，它可维持细胞在致癌转化途中的存活并成为治疗性抗性的基础。最近的研究表明，程序性细胞死亡不仅限于caspase依赖性凋亡，还包括坏死性坏死（necroptosis），这是一种由受体相互作用蛋白1（RIP1），RIP3和混合谱系激酶结构域类似（MLKL）蛋白控制的坏死性死亡。坏死性坏死是对严重压力和阻断细胞凋亡的关键细胞杀伤机制，并可由炎性细胞因子或化学治疗药物诱导。在人类肿瘤中经常发现诸如RIP3和柱状增生病（CYLD）的坏死病调节因子的遗传或表观遗传学改变。与细胞凋亡不同，坏死病可引起更强大的免疫反应，可通过消除引起肿瘤的突变和病毒来充当防御机制。此外，当前正在临床开发中的几类抗癌药，例如SMAC和BH3模拟物，除了可以凋亡外，还可以促进坏死性肾病。对坏死，凋亡和其他细胞死亡方式之间相互作用的更完整理解对于开发新的治疗策略以增强对肿瘤细胞的杀伤力至关重要。 （C）2016 Elsevier B.V.保留所有权利。

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