Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Madrid 28049, Spain.
Nat Rev Cancer. 2011 Dec 15;12(1):23-38. doi: 10.1038/nrc3169.
After years of extensive scientific discovery much has been learned about the networks that regulate epithelial homeostasis. Loss of expression or functional activity of cell adhesion and cell polarity proteins (including the PAR, crumbs (CRB) and scribble (SCRIB) complexes) is intricately related to advanced stages of tumour progression and invasiveness. But the key roles of these proteins in crosstalk with the Hippo and liver kinase B1 (LKB1)-AMPK pathways and in epithelial function and proliferation indicate that they may also be associated with the early stages of tumorigenesis. For example, deregulation of adhesion and polarity proteins can cause misoriented cell divisions and increased self-renewal of adult epithelial stem cells. In this Review, we highlight some advances in the understanding of how loss of epithelial cell polarity contributes to tumorigenesis.
经过多年广泛的科学发现，人们对调节上皮细胞稳态的网络有了更多的了解。细胞黏附蛋白和细胞极性蛋白（包括 PAR、CRB 和 SCRIB 复合物）的表达或功能活性丧失与肿瘤进展和侵袭的晚期阶段密切相关。但是，这些蛋白在与 Hippo 和肝激酶 B1（LKB1）-AMPK 通路的相互作用以及在上皮细胞功能和增殖中的关键作用表明，它们也可能与肿瘤发生的早期阶段有关。例如，黏附蛋白和极性蛋白的失调会导致细胞分裂方向错误，并增加成年上皮干细胞的自我更新。在这篇综述中，我们强调了对上皮细胞极性丧失如何促进肿瘤发生的理解的一些进展。
