Asymmetric cell division and template DNA co-segregation in cancer stem cells.
Asymmetric cell division and template DNA co-segregation in cancer stem cells.
复制标题
DOI：
10.3389/fonc.2014.00226
复制
发表时间：
2014
影响因子：
4.7
通讯作者：
Liu W
中科院分区：
文献类型：
--
作者：
Pine SR;Liu W
在组织稳态期间，正常干细胞通过一系列仔细控制的对称和不对称细胞分裂（ACD）自我更新并重新填充组织内发现的不同细胞类型。实体瘤包括具有失调的自我更新和过度对称细胞分裂的癌症干细胞（CSC）的子集的概念已经导致了许多旨在阐明在稳态条件下、在干细胞扩增期间和在癌症中调节ACD的机制的研究。从这个角度来看，我们专注于ACD过程中可以建立的一种不对称性，称为模板DNA的非随机共分离，它已经在许多物种，细胞类型和癌症中被发现。我们讨论的作用，p53损失在维持自我更新的正常和恶性细胞。然后，我们回顾了我们目前的知识的模板DNA链的共分离的机制和干细胞通路与它在正常和CSC。
During tissue homeostasis, normal stem cells self-renew and repopulate the diverse cell types found within the tissue via a series of carefully controlled symmetric and asymmetric cell divisions (ACDs). The notion that solid tumors comprise a subset of cancer stem cells (CSCs) with dysregulated self-renewal and excessive symmetric cell divisions has led to numerous studies aimed to elucidate the mechanisms regulating ACD under steady-state conditions, during stem-cell expansion and in cancer. In this perspective, we focus on a type of asymmetry that can be established during ACD, called non-random co-segregation of template DNA, which has been identified across numerous species, cell types, and cancers. We discuss the role of p53 loss in maintaining self-renewal in both normal and malignant cells. We then review our current knowledge of the mechanisms underlying co-segregation of template DNA strands and the stem-cell pathways associated with it in normal and CSCs.