Epigenetic mechanism of survivin dysregulation in human cancer.
Epigenetic mechanism of survivin dysregulation in human cancer.
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DOI：
10.1007/s11427-017-9230-2
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发表时间：
2018-07
期刊：
影响因子：
--
通讯作者：
Liu B
中科院分区：
文献类型：
--
作者：
Lyu H;Huang J;He Z;Liu B
Survivin（编码基因BIRC 5）是一种具有双重功能的蛋白质，作为细胞凋亡的关键抑制剂（IAP）和细胞周期进程的关键调节剂起作用。它通常在发育过程中在胚胎组织中产生，并且在大多数成体组织中检测不到。Survivin的过表达经常发生在各种人类癌症中，并且增加的Survivin与较差的临床结果、肿瘤复发和治疗抗性相关。由于Survivin在肿瘤组织中特异性表达，而在正常组织中不表达，因此成为肿瘤治疗的一个新靶点。尽管几种靶向Survivin的治疗方法正在人类癌症的临床试验中积极进行，但迄今为止还没有Survivin靶向疗法被批准用于癌症治疗。大量的研究致力于揭示Survivin在转录和转录后调控等多个水平上调控异常的机制。现就Survivin在人类肿瘤中的表达及其转录和表观遗传调控作一综述。我们关注DNA甲基化和组蛋白修饰的影响，包括特定的赖氨酸甲基化，去甲基化和乙酰化对Survivin表达的影响。最后讨论了以Survivin为靶点的表观遗传学方法在肿瘤治疗中的最新进展。
Survivin (coding gene BIRC5) is a dual functional protein acting as a critical inhibitor of apoptosis (IAP) and key regulator of cell cycle progression. It is usually produced in embryonic tissues during development and undetectable in most adult tissues. Overexpression of Survivin frequently occurs in various human cancers and increased Survivin correlates with poor clinic outcome, tumor recurrence, and therapeutic resistance. Because of its selective expression in tumor, but not normal tissues, Survivin has been recognized as an attractive target for cancer treatment. Although several therapeutic approaches targeting Survivin are actively under clinical trials in human cancers, to date no Survivin-targeted therapy has been approved for cancer treatment. Numerous studies have devoted to uncover the underlying mechanism resulting in Survivin dysregulation at multiple levels, such as transcriptional and post-transcriptional regulation. The current article provides a literature review on the transcriptional and epigenetic regulation of Survivin expression in human cancers. We focus on the impact of DNA methylation and histone modifications, including specific lysine methylation, demethylation, and acetylation on the expression of Survivin. The latest development of epigenetic approaches targeting Survivin for cancer treatment are also discussed.
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影响因子：
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作者：
Kim JS;Kim HA;Seong MK;Seol H;Oh JS;Kim EK;Chang JW;Hwang SG;Noh WC
通讯作者：
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影响因子：
11.5
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通讯作者：
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