The role of apoptosis-induced proliferation for regeneration and cancer.
The role of apoptosis-induced proliferation for regeneration and cancer.
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DOI：
10.1101/cshperspect.a008797
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发表时间：
2012-08-01
影响因子：
7.2
通讯作者：
Bergmann A
中科院分区：
文献类型：
--
作者：
Ryoo HD;Bergmann A
致力于杀死细胞的基因一定是因为它们对有机体生存的积极影响而进化的。凋亡基因的正功能已经在大量的生物学背景下得到很好的确立，包括它们在消除受损和潜在癌细胞中的作用。最近，有证据表明，促凋亡蛋白（主要是半胱天冬酶）可以诱导邻近存活细胞的增殖，以取代垂死细胞。这个过程，我们称之为“骨肉瘤诱导的增殖”，可能对干细胞活性和组织再生至关重要。根据所涉及的半胱天冬酶，至少可以区分两种不同类型的骨化诱导的增殖。这些类型之一已经使用一种模型进行了研究，在该模型中，细胞已经启动了细胞死亡，但是由于效应物半胱天冬酶抑制而被阻止执行细胞死亡，从而产生发出持续的有丝分裂原信号和过度生长的“不死”细胞。这种情况可能导致某些形式的癌症。在这篇综述中，我们总结了目前的知识，乳腺癌诱导的增殖，并讨论其组织再生和癌症的相关性。
Genes dedicated to killing cells must have evolved because of their positive effects on organismal survival. Positive functions of apoptotic genes have been well established in a large number of biological contexts, including their role in eliminating damaged and potentially cancerous cells. More recently, evidence has suggested that proapoptotic proteins—mostly caspases—can induce proliferation of neighboring surviving cells to replace dying cells. This process, that we will refer to as “apoptosis-induced proliferation,” may be critical for stem cell activity and tissue regeneration. Depending on the caspases involved, at least two distinct types of apoptosis-induced proliferation can be distinguished. One of these types have been studied using a model in which cells have initiated cell death, but are prevented from executing it because of effector caspase inhibition, thereby generating “undead” cells that emit persistent mitogen signaling and overgrowth. Such conditions are likely to contribute to certain forms of cancer. In this review, we summarize the current knowledge of apoptosis-induced proliferation and discuss its relevance for tissue regeneration and cancer.
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通讯作者：
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