E-cadherin expression: a counterbalance for cancer cell invasion.

摘要: Invasion, eventually leading to metastasis, is presented as the result of a balance between activation 2 sets genes, coined i+ (invasion promotor) and i- suppressor) genes. Experiments in vitro have indicated that homotypic homophilic epithelial cell--cell adhesion molecule E-cadherin (L-CAM; uvomorulin; cell CAM 120/80; Arc-1; rrl antigen) an gene product. In several families, manipulation at level protein by antibody-mediated inactivation, mRNA antisense DNA transfection, genome sense transfection respectively resulted induction suppression invasiveness. Nude mouse tumors from non-invasive homogeneously E-cadherin-positive populations were found be invasive metastatic. These expressed heterogeneous manner, undifferentiated cells being negative; but tumor-derived culture again E-cadherin-positive, indicating downregulation this host factors. Several types human cancers showed similar heterogeneity suggesting relationship invasion. Our current research focus on factors responsible for experimental cancers.