title: Intercellular adhesion molecule-1 is upregulated via the protein kinase C pathway in human thyroid carcinoma cell lines.
abstract: Nonantigen specific adhesion systems lymphocyte function-associated antigen 1/intercellular adhesion molecule (LFA-1/ICAM-1) and cluster designation 2/lymphocyte function-associated antigen 3 (CD2/LFA-3) are considered a crucial step in immune-mediated cell-cell adhesion reactions. In particular, the LFA-1/ICAM-1 system is deeply involved in major histocompatibility system (MHC)-restricted and non-MHC-restricted cellular cytotoxicity of effector cells against cancer tissues. We have investigated in human thyroid carcinoma cell lines the role of the protein kinase C (PKC) pathway on ICAM-1 expression. Incubation with tissue plasminogen activator (TPA), an agonist of PKC, of two papillary (NPA and TPC-1) and one anaplastic (ARO) carcinoma cell lines induced an ICAM-1 upregulation of both protein and mRNA production. This phenomenon was dependent on RNA and protein synthesis and was inhibited by PKC antagonists such as staurosporine and H-7. A parallel increase in the soluble form of ICAM-1 followed the upregulation of cellular ICAM-1 levels induced by TPA. In conclusion, the PKC pathway is involved in the regulation of ICAM-1 expression in human thyroid carcinoma cell lines. Further studies are necessary to clarify the effects of the PKC pathway on the diffusion of thyroid tumors.
authors.affiliation: Dipartimento di Endocrinologia ed Oncologia Molecolare e Clinica, Università degli Studi di Napoli "Federico II", Facoltà di Medicina e Chirurgia, Naples, Italy.
authors.forename: V
authors.initials: V
authors.lastname: Bassi
authors.forename: S
authors.initials: S
authors.lastname: De Riu
authors.forename: A
authors.initials: A
authors.lastname: Feliciello
authors.forename: M
authors.initials: M
authors.lastname: Altomonte
authors.forename: G
authors.initials: G
authors.lastname: Allevato
authors.forename: G
authors.initials: G
authors.lastname: Rossi
authors.forename: G F
authors.initials: GF
authors.lastname: Fenzi
mesh_terms: D015152:Blotting, Northern; D002277:Carcinoma / Q000378:metabolism* / Q000473:pathology; D002291:Carcinoma, Papillary / Q000378:metabolism* / Q000473:pathology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism*; D009363:Neoplasm Proteins / Q000096:biosynthesis; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000378:metabolism*; D012313:RNA / Q000096:biosynthesis; D012333:RNA, Messenger / Q000378:metabolism; D012995:Solubility; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D013964:Thyroid Neoplasms / Q000378:metabolism* / Q000473:pathology; D014407:Tumor Cells, Cultured / Q000187:drug effects / Q000378:metabolism
chemical_list: D004791:Enzyme Inhibitors; D009363:Neoplasm Proteins; D012333:RNA, Messenger; D018799:Intercellular Adhesion Molecule-1; D012313:RNA; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate