Interleukin 1 promotes tumor cell adhesion to cultured human endothelial cells.

Abstract

We report that IL 1 acts on the endothelium, inducing a longlasting increase in its adhesivity to tumor cells. Selective pretreatment of cultured human umbilical vein endothelial cells (EC) with IL 1 caused a significant increase in adhesion of three human colorectal carcinoma (HT-29, HCC-P2988, and HCC-M1410) cell lines and one human melanoma (A-375) cell line. Tumor necrosis factor (TNF) was as effective as IL 1 in promoting tumor cell adhesion to EC, whereas IFN Y and IL 2 were inactive. The IL 1 and TNF induction of EC adhesivity was both concentration (threshold concentration 1 U/ml) and time dependent (peak 4-6 h), reversible within 24 h, and blocked by a protein synthesis inhibitor. The IL 1 and TNF action on EC may play a role in tumor cell lodgment.

Rolling and adhesion of human tumor cells on vascular endothelium under physiological flow conditions.

“…1% bovine serum albumin, referred to as test medium. HUVEC were isolated from the human umbilical vein and grown in culture as previously described ( 16,31 ). Cells were grown in M 199 medium supplemented with 10% fetal calf serum and 10% human serum.…”

“…Adhesion of tumor cells is significantly augmented on EC activated by cytokines (16)(17)(18). This results from the induction, or enhanced expression, of adhesion molecules on EC, as described for the adhesion of leukocytes on EC (19).…”

“…The adhesion of six human tumor lines of different histological origin was investigated at different shear stresses. The specific adhesion mechanisms involved in this process were evaluated using two representative tumor types, the colon carcinoma HT-29M and the melanoma A375M, already described as adhering on cytokine-activated EC preferentially through selectin-or integrin-mediated pathways ( 16,22,25 ). We also investigated the selective interaction of tumor cells with E-selectin and VCAM-1 molecules immobilized on artificial surfaces using the same flow chamber.…”

Tumour-derived interleukin 1α (IL-1α) up-regulates the release of soluble intercellular adhesion molecule-1 (sICAM-1) by endothelial cells

“…The increase in sICAM-1 release by HUVECs was significantly (P = 0.02, data not shown) higher with CM from 5637 cells than with CM from HT-1080 and was completely abolished by anti-IL-la neutralizing antibodies. In addition, using (Dejana et al, 1988) or tumour-derived (Burrow et al, 1991;Kaji et al, 1995) ILla increases the adhesion of neoplastic cells to HUVECs in vitro and enhances the metastatic potential of neoplastic cells (Giavazzi et al, 1990), and that IL-1 receptor blockade reduces the number and the size of metastases (Vidal-Vanaclocha et al, 1994). These tumour spread-promoting effects of IL-la are independent from endothelial ICAM-1 because of the absence of LFA-1 in solid malignancies (Altomonte et al, 1993;Futagami-Mizoguchi et al, 1993).…”

TLR2 Limits Development of Hepatocellular Carcinoma by Reducing IL18-Mediated Immunosuppression

“…IL1b and IL18, both of which belong to the IL1 superfamily and are products of inflammasome activation, have been shown to be important in tumorigenesis. In mice, IL1b promotes metastasis (5) and tumor cell adhesion to endothelial cells (6). In patients with chronic hepatitis C virus (HCV) infection, the IL1b-31 genotype T/T and the IL1b-511/-31 haplotype C-T associate with HCC occurrence (7).…”