KAI1/CD82 over-expression in non-small cell lung carcinoma cells suppresses tumor invasiveness and metastatic potential by inducing matrix metalloproteinase-9 inactivation via up-regulation of tissue inhibitor of metalloproteinase-1 (TIMP-1).

KAI1/CD82 decreased the metastatic phenotype of H1299 lung carcinoma cells by down-regulating Rac1 expression through the PI3K/Akt/mTOR pathway.

Angiogenesis and the expressions of CD82 and HIF-1alpha are related to differentiation, lymph node metastasis and clinical staging in non-small cell lung cancer.

The low expression of CD82/KAI1 and E-cadherin was closely related to the invasion, progression and metastasis of non-small cell lung cancer.

High KAI1 expression is associated with epithelial-mesenchymal transition in non-small cell lung cancer.