Yabut Odessa R, Pleasure Samuel J
Department of Neurology, University of California San Francisco, San Francisco, California, USA.
Programs in Neuroscience and Developmental Biology, Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California San Francisco, California, USA.
Opera Med Physiol. 2016 Dec;2(3-4):181-187. doi: 10.20388/omp2016.003.0040. Epub 2016 Dec 25.
Isolated brain tumors contain cells that exhibit stem cell features and a tissue microenvironment bearing remarkable similarities to the normal neurogenic niche. This supports the idea that neural stem (NSCs) or progenitor cells, and their progeny are the likely tumor cell(s) of origin. This prompted the investigation of the relationship between NSCs/progenitors and the initiation of tumorigenesis. These studies led to the identification of common signaling machineries underlying NSC development and tumor formation, particularly those with known roles in proliferation and cell fate determination. This review will explore the molecular mechanisms that regulate NSC behavior in the neurogenic niche of the forebrain, and how deregulation of the developmental potential of NSCs might contribute to tumorigenesis.
孤立性脑肿瘤包含具有干细胞特征的细胞以及与正常神经发生微环境具有显著相似性的组织微环境。这支持了神经干细胞(NSCs)或祖细胞及其后代可能是肿瘤起源细胞的观点。这促使人们对NSCs/祖细胞与肿瘤发生起始之间的关系进行研究。这些研究导致了在NSC发育和肿瘤形成中潜在的共同信号机制的鉴定,特别是那些在增殖和细胞命运决定中具有已知作用的机制。本综述将探讨在前脑神经发生微环境中调节NSC行为的分子机制,以及NSCs发育潜能的失调如何可能导致肿瘤发生。