As a barrier to metastasis of cancer, cells that lost contact with the 
neighbouring cells or extracellular matrix(Extracellular matrix, ECM) will be 
subjected to apoptosis. This cell death process has been termed "anoikis". When 
normal epithelial cells or solid tumor cells without metastatic potential detach 
from the primary site, and then enter into the circulatory system, the anoikis 
mechanism will be activated. The significance of anoikis is to prevent the 
shedding cells from growing and implanting into other inappropriate sites. Tumor 
cells, especially several malignant cells that is prone to transfer to distant 
sites, have properties of anti-anoikis, which facilitates metastasis as well as 
invasion of tumor cells. The studies found that tumor cells can resist anoikis 
through multiple mechanisms: the pro-survival pathways are activated by cells 
autocrine growth factors and paracrine factors derived from neighboring cells; 
cells change the pattern of integrin expression so that they can receive 
survival signals from new environment; reactive oxygen species (ROS) activates 
growth factor receptors in a ligand-independent way to avoid apoptosis; and 
epithelial-mesenchymal transformation(EMT) is activated etc.. All of these 
mechanisms lead to activation of survival signals and inhibition of apoptotic 
pathways, and ultimately cause resistance to anoikis as well as metastasis. This 
paper summarizes the key mechanisms of the current studies on metastasis, which 
also suggest important targets for cancer therapy.