Abstract:
Tensin 1 was originally described as a focal adhesion adaptor protein, playing a role in extracellular matrix and cytoskeletal interactions. Three other Tensin proteins were subsequently discovered, and the family was grouped as Tensin. It is now recognized that these proteins interact with multiple cell signalling cascades that are implicated in tumorigenesis. To understand the role of Tensin 1-3 in neoplasia, current molecular evidence is categorized by the hallmarks of cancer model. Additionally, clinical data involving Tensin 1-3 are reviewed to investigate the correlation between cellular effects and clinical phenotype. Tensin proteins commonly interact with the tumour suppressor, DLC1. The ability of Tensin to promote tumour progression is directly correlated with DLC1 expression. Members of the Tensin family appear to have tumour subtype-dependent effects on oncogenesis; despite numerous data evidencing a tumour suppressor role for Tensin 2, association of Tensins 1-3 with an oncogenic role notably in colorectal carcinoma and pancreatic ductal adenocarcinoma is of potential clinical relevance. The complex interplay between these focal adhesion adaptor proteins and signalling pathways are discussed to provide an up to date review of their role in cancer biology.
摘要:
Tensin1最初被描述为粘着斑衔接蛋白,在细胞外基质和细胞骨架相互作用中发挥作用。随后发现了另外三种Tensin蛋白,这个家族被归类为Tensin。现在认识到这些蛋白质与涉及肿瘤发生的多个细胞信号传导级联相互作用。了解Tensin1-3在肿瘤形成中的作用,当前的分子证据被癌症模型的标志分类。此外,我们回顾了涉及Tensin1-3的临床数据,以研究细胞效应与临床表型之间的相关性。Tensin蛋白通常与肿瘤抑制因子相互作用,DLC1。Tensin促进肿瘤进展的能力与DLC1表达直接相关。Tensin家族的成员似乎对肿瘤发生具有肿瘤亚型依赖性作用;尽管有许多数据证明Tensin2具有肿瘤抑制作用,但Tensin1-3与致癌作用的关联尤其是在结直肠癌和胰腺导管腺癌中具有潜在的临床意义。讨论了这些粘着斑衔接蛋白与信号通路之间的复杂相互作用,以提供它们在癌症生物学中的作用的最新综述。