| Autor: |
Fiore APZP; e-Signal Laboratory, Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, Brazil., Ribeiro PF; e-Signal Laboratory, Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, Brazil., Bruni-Cardoso A; e-Signal Laboratory, Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, Brazil. |
| Jazyk: |
angličtina |
| Zdroj: |
Frontiers in cell and developmental biology [Front Cell Dev Biol] 2018 Jun 07; Vol. 6, pp. 59. Date of Electronic Publication: 2018 Jun 07 (Print Publication: 2018). |
| DOI: |
10.3389/fcell.2018.00059 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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