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首页> 外文期刊>Cell cycle >The anaphase promoting complex: a critical target for viral proteins and anti-cancer drugs.
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The anaphase promoting complex: a critical target for viral proteins and anti-cancer drugs.

机译：后期促进复合物：病毒蛋白和抗癌药物的关键靶标。

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摘要

The study of animal viruses has provided extraordinary insights into cell cycle dynamics and tumor biology. The significance of the p53 and Rb tumor suppressor proteins, for example, was discovered due to their interactions with viral oncogenes. In the past several years, investigations with four viral proteins, human immunodeficiency virus type 1 (HIV-1) vpr, adenovirus E4orf4, chicken anemia virus (CAV) apoptin and human T lymphotropic virus type I (HTLV-I) Tax, have indicated that there are also critical viral targets involved in G2/M control. In particular, recent studies with E4orf4 and apoptin have shown that they induce G2/M arrest by targeting and inhibiting the anaphase-promoting complex/cyclosome (APC/C). Notably, these two viral proteins induce apoptosis selectively in transformed cells in a p53-independent manner; thus pathways affected by these proteins are of significant therapeutic interest. Further investigation of the underlying mechanism of G2/M arrest and subsequent apoptosis inducedby viral APC/C inhibitors may shed light on the mechanisms of current cancer therapies and provide the foundation for developing novel therapeutic targets.
机译：动物病毒的研究为细胞周期动力学和肿瘤生物学提供了非凡的见解。例如，由于p53和Rb肿瘤抑制蛋白与病毒癌基因的相互作用而被发现具有重要意义。在过去的几年中，对四种病毒蛋白，人类免疫缺陷病毒1型（HIV-1）vpr，腺病毒E4orf4，鸡贫血病毒（CAV）凋亡蛋白和人类T淋巴病毒I型（HTLV-1）税的调查表明G2 / M控制中也涉及关键的病毒靶标。特别是，最近对E4orf4和细胞凋亡素的研究表明，它们通过靶向和抑制促后期合成物/环体（APC / C）诱导G2 / M阻滞。值得注意的是，这两种病毒蛋白以不依赖p53的方式选择性诱导转化细胞凋亡。因此，受这些蛋白质影响的途径具有重要的治疗意义。进一步研究病毒APC / C抑制剂诱导的G2 / M阻滞和随后的细胞凋亡的潜在机制，可能为当前癌症治疗的机制提供启示，并为开发新的治疗靶标奠定基础。

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