Abstract
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.