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The difference between human normal and carcinoma lung cells was studied with regard to the protein expression level and localization of the cadherin/catenin/actin complex. Results demonstrated that normal lung cell RF expressed high levels of N-cadherin, β-catenin, α-catenin. These 3 proteins were colocalized at AJs and their submembrane adhesion plaques where they link the Rho-phalloidin-positive actin stress fibers, indicating the existence of N-cadherin/catenin/actin complexes at the AJs. Aberrant expression of AJ proteins and the actin cytoskelecton in carcinoma PG cells was observed: (1) inhibition of N-cadherin and to a degree of inhibition of α-catenin protein expression; (2) varied protein modification of β-catenin in cytoplasm soluble fraction and altered distribution of immunofluorescence: majorly in the cytoplasm and minorly on the membrane; (3) disassembly of actin stress fibers and formation of actin bodies in the cytoplasm. The data suggest that inhibited expression of AJ proteins is correlated with the disruption of the AJ complexes and the actin cytoskeleton in carcinoma PG cells, and responsible for its metastasis behaviors.
The difference between human normal and carcinoma lung cells was studied with regard to the protein expression level and localization of the cadherin/catenin/actin complex. Results demonstrated that normal lung cell RF expressed high levels of N-cadherin, β-catenin, α- Catenin. These 3 proteins were colocalized at AJs and their submembrane adhesion plaques where they link the Rho-phalloidin-positive actin stress fibers, indicating the existence of N-cadherin/catenin/actin complexes at the AJs. Aberrant expression of AJ proteins and the Actin cytoskelecton in carcinoma PG cells was observed: (1) inhibition of N-cadherin and to a degree of inhibition of α-catenin protein expression; (2) varied protein modification of β-catenin in cytoplasm soluble fraction and altered distribution of immunofluorescence: The majorly in the cytoplasm and minorly on the membrane; (3) disassembly of actin stress fibers and formation of actin bodies in the cytoplasm. The data suggest that inhibited expression Of AJ proteins is correlated with the disruption of the AJ complexes and the actin cytoskeleton in carcinoma PG cells, and responsible for its metastasis behaviors.