1α,25-dihydroxyvitamin D3 modulates the interaction between immune and colon cancer cells

被引:26
作者
Bessler, Hanna
Djaldetti, Meir [1 ]
机构
[1] Hasharon Hosp, Rabin Med Ctr, Lab Immunol & Hematol Res, IL-49372 Petah Tiqwa, Israel
关键词
Experimental; Vitamin D; Peripheral blood mononuclear cells; Cytokines; Colon cancer cells; VITAMIN-D;
D O I
10.1016/j.biopha.2012.06.005
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Following observations indicating the existence of a relationship between immune and cancer cells in the course of tumor development, it was the aim of the study to establish the role of 1 alpha,25-dihydroxyvitamin D3 (vit. D) in the functional equilibrium between cells from two human colon carcinoma lines-induced cytokine production by peripheral blood mononuclear cells (PBMC). PBMC were incubated with HT-29 and RKO human colon cancer cells with and without vit. D at final concentrations of 10 (8), 10 (7) or 10 (6) M. The production of the cytokines TNF-alpha, IL-6 and IL-10, as well as the effect of the vitamin on tumor cell proliferation were evaluated. Incubation of PBMC with either HT-29 or RKO cells caused a significant stimulation of both pro- and anti-inflammatory cytokine generation. Addition of vit. D to the incubation mixture containing PBMC and cells of both colon carcinoma lines caused a marked inhibition of the generation of the pro-inflammatory cytokines TNF-alpha and IL-6 and to a lesser extent-of the IL-10. Vit. D did not affect the proliferation of the cancer cells. The results indicate the existence of a functional "dialog" between immune and cancer cells expressed by an alteration of their capacity for cytokine production and support the role of inflammation in carcinogenesis. The ability of vit. D to attenuate production of the pro-inflammatory cytokines when added to the incubation mixture containing PBMC and cancer cells endorses observations as for the beneficial role of the vitamin in suppressing inflammation with subsequent colon cancer prevention. (C) 2012 Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:428 / 432
页数:5
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