THE EXPRESSION OF ICAM-1 AND VCAM-1 IS REGULATED BY IL-1 AND DOUBLE-STRANDED RNA IN KAPOSI'S SARCOMA CELLS (MEETING ABSTRACT)

Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.

THE EXPRESSION OF ICAM-1 AND VCAM-1 IS REGULATED BY IL-1 AND DOUBLE-STRANDED RNA IN KAPOSI'S SARCOMA CELLS (MEETING ABSTRACT)

Proc Annu Meet Am Assoc Cancer Res; 33:A202 1992. Unique Identifier : AIDSLINE ICDB/92682737
Yang J; Xu Y; Hagan MK; Offermann MK; Winship Cancer Center, Emory Univ. Sch. of Medicine, Atlanta, GA; 30322

Abstract: Kaposi's sarcoma (KS), a neoplasm with multifocal vascular lesions, is often seen in homosexual HIV-infected patients. Evidence exists that disordered regulation and expression of cytokines and other agents contribute to abnormal proliferation of KS cells. Inflammatory cells are present in lesions of all stages, especially early stage lesions. These inflammatory cells are likely sources of agents involved in the development or progression of KS. Since cells expressing adhesion molecules, including ICAM-1 and VCAM-1, promote adhesion of inflammatory cells, we have investigated the ability of KS cells to express cell surface adhesion molecules, both in the basal state and in response to inducing agents. In the absence of inducers, KS cells express low levels of ICAM-1 and undetectable VCAM-1. Treatment of KS cells with the synthetic double-stranded RNA, poly I:C, induces ICAM-1 and VCAM-1 expression at both mRNA and cell surface protein levels. IL1 beta also induces these genes. However, poly I:C leads to more sustained increases in ICAM-1 and VCAM-1 than IL-1 beta. This suggests that in vivo, viruses with double-stranded RNA intermediates could induce ICAM-1 and VCAM-1 in KS cells or in their precursors, thereby initiating a cascade of inflammatory cell adhesion to these cells. Agents released from these inflammatory cells could then potentiate the development of the KS.

Keywords: Antigens, CD/GENETICS Cell Adhesion Molecules/*GENETICS Gene Expression/DRUG EFFECTS Gene Expression Regulation, Neoplastic/DRUG EFFECTS Human Inflammation Interleukin-1/*PHARMACOLOGY Poly I-C/*PHARMACOLOGY RNA, Double-Stranded/*PHARMACOLOGY Sarcoma, Kaposi's/GENETICS/*PHYSIOPATHOLOGY Tumor Cells, Cultured ABSTRACT
920730
M9271100

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