Influence of Cytokines on the Expression of Fas Ligand and CD44 Splice Variants in Colon Carcinoma Cells

Abstract

The expression of Fas ligand (FasL) by malignant cells might be a mechanism for tumor immune escape. We investigated FasL expression by LS 174T colon carcinoma cells. Furthermore, the effects of in vitro stimulation with rIL-2, rIFN-γ and rTNF-α were investigated with regard to a possible regulation of the FasL expression by cytokines. FasL expression was detected by flow cytometry and RT-PCR. We observed a spontaneous expression of FasL by LS 174T cells. Incubation with high-dose rTNF-α induced an upregulation of FasL of 23%. rIL-2 and rIFN-γ did not significantly affect FasL expression. To control whether our cytokine stimulation experiments were suitable to prove an upregulation of membrane proteins by tumor cells, we investigated the expression of ICAM-1, N-CAM, CD44s, CD44v6 and CD44v10. These adhesion molecules were spontaneously expressed by LS 174T cells. Only ICAM-1 and CD44v10 were significantly upregulated by rIFN-γ and rTNF-α, respectively. These results could indicate that cytokines, released by tumor-infiltrating leukocytes, may induce the FasL-dependent apoptotic signal by which tumors downregulate an immunological host response.

Differential and Mutually Exclusive Expression of CD95 and CD95 Ligand in Epithelia of Normal Pancreas and Chronic Pancreatitis

“…The question arises whether this transfection restored physiologic levels or led to overexpression of STAT-1. In LS174T human colon carcinoma cells, constitutive CD95L expression was up-regulated by high-dose TNF␣, whereas IFN␥ or IL-2 failed to modulate CD95L (Wimmenauer et al, 1999). In critical conclusion, it is too early to generalize the fact that IFN␥ down-modulates CD95L transcripts and protein in AsPc1 and BxPc3 cells.…”

Attack the Tumor Counterattack-C-Flip Expression in Jurkat-T-Cells Protects Against Apoptosis Induced by Coculture with SW620 Colorectal Adenocarcinoma Cells

“…In order to demonstrate the expression of the transmembrane protein, FAS-ligand, in SW620 colorectal adenocarcinoma cells [34], we performed a detection procedure utilizing a primary FAS-Ligand antibody (N-20; Santa Cruz) and an infrared-conjugated secondary antibody (Alexa Fluor 633; Invitrogen) (Fig. 2).…”

Histoire naturelle et facteurs de risque du cancer colorectal au cours des maladies inflammatoires intestinales

“…L'inflammation colique chronique peut jouer un rôle favorisant de la carcinogenèse via au moins deux mécanismes. Le premier implique la production de cytokines proinflammatoires, telles que le TNF-α, l'IL-lβ, l'IL-6, ou la chémokine IL-8, molécules capables d'empêcher la glycolysation des glycoprotéines de la bordure en brosse des colonocytes [15][16][17]. Cette modification chimique conduit à une prolifération des cellules épithéliales en réponse à toute une série de lectines [18].…”