title: Decrease in gamma-actin expression, disruption of actin microfilaments and alterations in cell adhesion systems associated with acquisition of metastatic capacity in human salivary gland adenocarcinoma cell clones.
abstract: In order to clarify how cytoskeletons and adhesion systems change through acquisition of metastatic capacity in a cancer cell, we examined the expressions of beta- and gamma-actin, the morphology of actin microfilaments and focal contacts, and also the expression of vinculin in a salivary gland adenocarcinoma cell clone cl-1, which acquired metastatic capacity, in comparison with its original clone HSGc lacking metastatic ability. Two-dimensional gel electrophoresis of Triton-insoluble fractions and combined Western blot analysis by immunostaining with anti actin-isoform antibodies showed that the expression of gamma-actin was somewhat lower than that of beta-actin in HSGc, and cl-1 expressed a comparable amount of beta-actin to HSGc, whereas gamma-actin expression by cl-1 was far less than that by HSGc. Northern blot analysis demonstrated that there was little difference in the level of beta-actin mRNA between HSGc and cl-1, while the level of gamma-actin was markedly decreased in cl-1 as compared with HSGc. In terms of morphology, cl-1 cells showed disruption of actin microfilaments and a decrease in the size and number of focal contacts on the cell surface. Furthermore, cl-1 showed decreased expression of vinculin, which became obscured even at the end of actin microfilaments. These results demonstrated that a decrease in gamma-actin, disruption of actin microfilaments, and suppression of focal contacts as well as vinculin take place in the transformation from a non-metastatic condition to a metastatic one in the human salivary gland adenocarcinoma cell clones. Thus, it was strongly suggested that these changes contribute to a decrease in cell adhesiveness and an increase in cell motility, which is probably a major cause for acquisition of metastatic potential.
authors.affiliation: Department of Otorhinolaryngology, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba, 260, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Suzuki
authors.forename: H
authors.initials: H
authors.lastname: Nagata
authors.forename: Y
authors.initials: Y
authors.lastname: Shimada
authors.forename: A
authors.initials: A
authors.lastname: Konno
mesh_terms: D008841:Actin Cytoskeleton / Q000473:pathology* / Q000648:ultrastructure; D000199:Actins / Q000096:biosynthesis* / Q000378:metabolism / Q000648:ultrastructure; D000230:Adenocarcinoma / Q000473:pathology* / Q000503:physiopathology / Q000648:ultrastructure; D015153:Blotting, Western; D002448:Cell Adhesion; D002999:Clone Cells; D015180:Electrophoresis, Gel, Two-Dimensional; D005455:Fluorescent Antibody Technique; D006801:Humans; D009362:Neoplasm Metastasis; D012468:Salivary Gland Neoplasms / Q000473:pathology* / Q000503:physiopathology / Q000648:ultrastructure; D014407:Tumor Cells, Cultured; D016596:Vinculin / Q000096:biosynthesis
chemical_list: D000199:Actins; D016596:Vinculin