Fiore Ana Paula Zen Petisco, Ribeiro Pedro de Freitas, Bruni-Cardoso Alexandre
e-Signal Laboratory, Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, Brazil.
Front Cell Dev Biol. 2018 Jun 7;6:59. doi: 10.3389/fcell.2018.00059. eCollection 2018.
Cells from prokaryota to the more complex metazoans cease proliferating at some point in their lives and enter a reversible, proliferative-dormant state termed quiescence. The appearance of quiescence in the course of evolution was essential to the acquisition of multicellular specialization and compartmentalization and is also a central aspect of tissue function and homeostasis. But what makes a cell cease proliferating even in the presence of nutrients, growth factors, and mitogens? And what makes some cells "wake up" when they should not, as is the case in cancer? Here, we summarize and discuss evidence showing how microenvironmental cues such as those originating from metabolism, extracellular matrix (ECM) composition and arrangement, neighboring cells and tissue architecture control the cellular proliferation-quiescence decision, and how this complex regulation is corrupted in cancer.
从原核生物到更复杂的后生动物，细胞在其生命的某个阶段会停止增殖，并进入一种可逆的、增殖休眠状态，即静止期。静止期在进化过程中的出现对于多细胞特化和区室化的获得至关重要，也是组织功能和稳态的核心方面。但是，是什么使得细胞即使在有营养物质、生长因子和有丝分裂原的情况下仍停止增殖呢？又是什么使得一些细胞在不应该的时候“苏醒”，比如在癌症中出现的情况呢？在这里，我们总结并讨论证据，这些证据表明诸如源自代谢、细胞外基质（ECM）组成和排列、相邻细胞以及组织结构等微环境线索如何控制细胞增殖 - 静止的决定，以及这种复杂的调节在癌症中是如何被破坏的。
