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Transduction of retinoic acid and gamma-interferon signal for intercellular adhesion molecule-1 expression on human tumor cell lines: evidence for the late-acting involvement of protein kinase C inactivation.
Cancer Res. 1993 Feb 15; 53(4):826-32.CR

Abstract

Intercellular adhesion molecule 1 (ICAM-1) is a major adhesion receptor of the immune system. Its cell surface expression on a wide variety of cells including cancer cells regulated by various proinflammatory cytokines. Incubation of the human glioma cell line HS 683 and the neuroblastoma cell line SK-N-SH with 12-phorbol 13-myristic acid (PMA), retinoic acid, or gamma-interferon (IFN-gamma) strongly stimulates ICAM-1 expression. In the present study, we investigated the role of the protein kinase C (PKC)-mediated signal transduction pathway in this process. We found that IFN-gamma, but not retinoic acid, was able to induce activation and translocation of PKC after 60 min in a dose-dependent fashion, contrasting with the very rapid activation and translocation induced by PMA which occurred at 15 min. The PKC inhibitors 1-(5-isoquinolinesulfonyl)-2-methyl-piperazine dihydrochloride and staurosporine, as well as depletion of PKC by a 24-h treatment with 100 nM PMA, decreased the PMA-mediated stimulation but not the retinoic acid- or the IFN-gamma-mediated stimulation of ICAM-1 expression. On the contrary, they rather stimulated ICAM-1 expression. Furthermore, this stimulation was additive with retinoic acid and IFN-gamma. A 24-h incubation in the presence of retinoic acid or IFN-gamma strongly inhibited activation and translocation of PKC by PMA. These results suggest that although PMA-induced ICAM-1 expression is PKC dependent on HS 683 and SK-N-SH cells, the stimulation of ICAM-1 expression by retinoic acid and by IFN-gamma may be due to PKC inactivation at longer time points (24 h), as mimicked by 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride, staurosporine, or PKC depletion by high doses of PMA.

Authors+Show Affiliations

Molecular Endocrinology Laboratory, CHUL Research Center, Québec, Canada.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8094032

Citation

Bouillon, M, and M Audette. "Transduction of Retinoic Acid and Gamma-interferon Signal for Intercellular Adhesion Molecule-1 Expression On Human Tumor Cell Lines: Evidence for the Late-acting Involvement of Protein Kinase C Inactivation." Cancer Research, vol. 53, no. 4, 1993, pp. 826-32.
Bouillon M, Audette M. Transduction of retinoic acid and gamma-interferon signal for intercellular adhesion molecule-1 expression on human tumor cell lines: evidence for the late-acting involvement of protein kinase C inactivation. Cancer Res. 1993;53(4):826-32.
Bouillon, M., & Audette, M. (1993). Transduction of retinoic acid and gamma-interferon signal for intercellular adhesion molecule-1 expression on human tumor cell lines: evidence for the late-acting involvement of protein kinase C inactivation. Cancer Research, 53(4), 826-32.
Bouillon M, Audette M. Transduction of Retinoic Acid and Gamma-interferon Signal for Intercellular Adhesion Molecule-1 Expression On Human Tumor Cell Lines: Evidence for the Late-acting Involvement of Protein Kinase C Inactivation. Cancer Res. 1993 Feb 15;53(4):826-32. PubMed PMID: 8094032.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Transduction of retinoic acid and gamma-interferon signal for intercellular adhesion molecule-1 expression on human tumor cell lines: evidence for the late-acting involvement of protein kinase C inactivation. AU - Bouillon,M, AU - Audette,M, PY - 1993/2/15/pubmed PY - 1993/2/15/medline PY - 1993/2/15/entrez SP - 826 EP - 32 JF - Cancer research JO - Cancer Res VL - 53 IS - 4 N2 - Intercellular adhesion molecule 1 (ICAM-1) is a major adhesion receptor of the immune system. Its cell surface expression on a wide variety of cells including cancer cells regulated by various proinflammatory cytokines. Incubation of the human glioma cell line HS 683 and the neuroblastoma cell line SK-N-SH with 12-phorbol 13-myristic acid (PMA), retinoic acid, or gamma-interferon (IFN-gamma) strongly stimulates ICAM-1 expression. In the present study, we investigated the role of the protein kinase C (PKC)-mediated signal transduction pathway in this process. We found that IFN-gamma, but not retinoic acid, was able to induce activation and translocation of PKC after 60 min in a dose-dependent fashion, contrasting with the very rapid activation and translocation induced by PMA which occurred at 15 min. The PKC inhibitors 1-(5-isoquinolinesulfonyl)-2-methyl-piperazine dihydrochloride and staurosporine, as well as depletion of PKC by a 24-h treatment with 100 nM PMA, decreased the PMA-mediated stimulation but not the retinoic acid- or the IFN-gamma-mediated stimulation of ICAM-1 expression. On the contrary, they rather stimulated ICAM-1 expression. Furthermore, this stimulation was additive with retinoic acid and IFN-gamma. A 24-h incubation in the presence of retinoic acid or IFN-gamma strongly inhibited activation and translocation of PKC by PMA. These results suggest that although PMA-induced ICAM-1 expression is PKC dependent on HS 683 and SK-N-SH cells, the stimulation of ICAM-1 expression by retinoic acid and by IFN-gamma may be due to PKC inactivation at longer time points (24 h), as mimicked by 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride, staurosporine, or PKC depletion by high doses of PMA. SN - 0008-5472 UR - https://www.unboundmedicine.com/medline/citation/8094032/Transduction_of_retinoic_acid_and_gamma_interferon_signal_for_intercellular_adhesion_molecule_1_expression_on_human_tumor_cell_lines:_evidence_for_the_late_acting_involvement_of_protein_kinase_C_inactivation_ L2 - http://cancerres.aacrjournals.org/cgi/pmidlookup?view=long&pmid=8094032 DB - PRIME DP - Unbound Medicine ER -