Journal
EUROPEAN JOURNAL OF CANCER
Volume 41, Issue 15, Pages 2347-2354Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.ejca.2005.07.014
Keywords
colon cancer; COGA cells; caco-2 cells; proliferation; interleukin-1; prostaglandins; IL-6 gene polymorphisms; IL-6 receptor-alpha; Gp130; STAT3
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Interleukin (IL)-6 mRNA expression in general is low in normal, adenomatous and cancerous human colon mucosa, except in rather undifferentiated lesions, in which IL-6 is overexpressed. Cytokeratin (CK) 8-positive carcinoma cells were identified by double immunostaining as almost exclusive source of IL-6. Likewise, in five (sub)clones of primary culture COGA-1 and COGA-13 human colon carcinoma cells, and in three established cell lines (Caco-2/AQ, Caco-2/15 and HT-29), efficient translation of IL-6 mRNA into protein was observed only in the least differentiated COGA-13 cells. Notably, IL-1 beta (5 ng/ml) enhanced IL-6 release in COGA-13 cultures by three orders of magnitude. Although all cell clones studied expressed the IL-6 receptor (IL-6R), rhIL-6 (1-100 ng/ml) had a significant effect on cellular proliferation only in highly differentiated Caco-2 cells. Our data imply that IL-6, when released from rather undifferentiated carcinoma cells, particularly in response to IL-1 beta, can advance tumour progression through paracrine growth stimulation of normal or highly differentiated colon tumour cells with intact STAT-3-mediated IL-6 signalling. (c) 2005 Elsevier Ltd. All rights reserved.
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