Exogenous expression of N-cadherin in breast cancer cells induces cell migration, invasion, and metastasis.

摘要: E- and N-cadherin are calcium-dependent cell adhesion molecules that mediate cell–cell also modulate migration tumor invasiveness. The loss of E-cadherin–mediated has been shown to play an important role in the transition epithelial tumors from a benign invasive state. However, recent evidence indicates another member cadherin family, N-cadherin, is expressed highly lines lacked E-cadherin expression. These findings have raised possibility contributes phenotype. To determine whether promotes invasion metastasis, we transfected weakly metastatic E-cadherin–expressing breast cancer line, MCF-7, with analyzed effects on migration, invasion, metastasis. Transfected cells both exhibited homotypic molecules. In vitro, N-cadherin–expressing migrated more efficiently, showed increased Matrigel, adhered efficiently monolayers endothelial cells. All produced low levels matrix metalloproteinase MMP-9, which was dramatically upregulated by treatment FGF-2 only Migration Matrigel were greatly enhanced this treatment. When injected into mammary fat pad nude mice, cells, but not control MCF-7 metastasized widely liver, pancreas, salivary gland, omentum, lung, lymph nodes, lumbar spinal muscle. expression maintained primary lesions. results demonstrate motility, metastasis even presence normally suppressive E-cadherin. increase MMP-9 production response growth factor may endow them greater ability penetrate protein barriers, while their adherence endothelium improve enter exit vasculature, two properties be responsible for