Department of Biology, Xavier University of Louisiana, 1 Drexel Drive, New Orleans, LA 70125, USA.
Cancer Lett. 2013 Jun 10;333(2):147-51. doi: 10.1016/j.canlet.2013.01.043. Epub 2013 Jan 31.
Epithelial cells and most adherent normal cells rely on adhesion-dependent, integrin-mediated survival signals from the extracellular matrix (ECM) to survive. When these cells are deprived of adhesion to the ECM, they undergo a specific form of apoptosis termed "anoikis." In contrast, malignant cells have attained mechanisms to enable them to survive in the absence of adhesion and are considered anchorage-independent. This review will focus on the biological function of the Bcl2-inhibitor of transcription (Bit1) protein in the anoikis process, the underlying molecular mechanism of Bit1 apoptotic function, and its role in tumor metastasis.
上皮细胞和大多数贴壁正常细胞依赖于细胞外基质(ECM)提供的、黏附依赖性的整合素介导的存活信号来维持生存。当这些细胞失去与 ECM 的黏附时,它们会经历一种特定形式的凋亡,称为“失巢凋亡”。相比之下,恶性细胞已经获得了在没有黏附的情况下存活的机制,因此被认为是不依赖于锚定的。本综述将重点介绍 Bcl2 转录抑制剂(Bit1)蛋白在失巢凋亡过程中的生物学功能、Bit1 凋亡功能的潜在分子机制及其在肿瘤转移中的作用。