Journal of Cancer Therapy

Volume 3, Issue 6 (November 2012)

ISSN Print: 2151-1934   ISSN Online: 2151-1942

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IL-6 Plays Crucial Roles in Sporadic Colorectal Cancer through the Cytokine Networks including CXCL7

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DOI: 10.4236/jct.2012.326112    4,188 Downloads   6,570 Views  Citations

ABSTRACT

IL-6 is a multifunctional cytokine and involved in variety of carcinogenesis. However, the association between IL-6 and sporadic colorectal cancer has not been fully explained. Here, we investigated the role of IL-6 signaling and the cytokine network in sporadic colorectal cancer. We investigated the serum IL-6 levels in patients with sporadic colorectal adenoma, cancer patients, and normal controls. In addition, the expressions of IL-6, gp130, and the IL-6 receptor subunit were investigated in biopsy specimens collected from these subjects. Furthermore, the expressions of CXCL7 and CXCR2, a chemokine and its receptor involved in IL-6 production, were also investigated. We observed an elevated level of serum IL-6 in colorectal cancer patients and an increased expression of IL-6 in colorectal cancer tissues, compared with the levels in a control group and in patients with adenoma. The phosphorylation of gp130 was also increased in the colorectal cancer tissues, compared with that in control and adenoma tissues. The expressions of CXCL7 and CXCR2 in the colorectal cancer tissues were also higher than those in control and adenoma tissues. IL-6 signaling is involved in sporadic colorectal cancer. In addition, the increased expressions of CXCL7 and CXCR2 might, in turn, increase the expression of IL-6 in colorectal cancer. Further studies are required to elucidate the function of the IL-6 signaling and the cytokine network in sporadic colorectal cancer.

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T. Uchiyama, H. Takahashi, H. Endo, E. Sakai, K. Hosono, Y. Nagashima and A. Nakajima, "IL-6 Plays Crucial Roles in Sporadic Colorectal Cancer through the Cytokine Networks including CXCL7," Journal of Cancer Therapy, Vol. 3 No. 6A, 2012, pp. 874-879. doi: 10.4236/jct.2012.326112.

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