HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Institute for Genetic Medicine >
Peer-reviewed Journal Articles, etc >

IL6 modulates the immune status of the tumor microenvironment to facilitate metastatic colonization of colorectal cancer cells

Files in This Item:
Cancer Immunol Res_18-0766.pdf1.9 MBPDFView/Open
Figure legend S1-S9.pdf90.83 kBPDFView/Open
Supplementary Figures 1-7.pptx32.62 MBMicrosoft Powerpoint XMLView/Open
Supplementary Figures 8-9.pptx15.13 MBMicrosoft Powerpoint XMLView/Open
Supplementary Tables 1-2.pptx52.13 kBMicrosoft Powerpoint XMLView/Open
Please use this identifier to cite or link to this item:

Title: IL6 modulates the immune status of the tumor microenvironment to facilitate metastatic colonization of colorectal cancer cells
Authors: Toyoshima, Yujiro Browse this author
Kitamura, Hidemitsu Browse this author →KAKEN DB
Xiang, Huihui Browse this author
Ohno, Yosuke Browse this author
Homma, Shigenori Browse this author →KAKEN DB
Kawamura, Hideki Browse this author →KAKEN DB
Takahashi, Norihiko Browse this author →KAKEN DB
Kamiyama, Toshiya Browse this author →KAKEN DB
Tanino, Mishie Browse this author →KAKEN DB
Taketomi, Akinobu Browse this author →KAKEN DB
Keywords: IL6
metastatic colonization
colorectal cancer
dendritic cells
cytotoxic T cells
Issue Date: Dec-2019
Publisher: American Association for Cancer Research (AACR)
Journal Title: Cancer Immunology Research
Volume: 7
Issue: 12
Start Page: 1944
End Page: 1957
Publisher DOI: 10.1158/2326-6066.CIR-18-0766
Abstract: It is unknown as to how liver metastases are correlated with host immune status in colorectal cancer. In this study, we found that IL-6, a proinflammatory cytokine produced in tumor-bearing states, promotes the metastatic colonization of colon cancer cells in association with dysfunctional anti-tumor immunity. In IL-6-deficient mice, metastatic colonization of CT26 cells in the liver was reduced, and the anti-tumor effector function of CD8+ T cells as well as IL-12 production by CD11c+ dendritic cells were augmented in vivo. Furthermore, IL-6-deficient mice exhibited enhanced IFNAR1- mediated type I interferon signaling, which upregulated PD-L1 and MHC class I expression on CT26 cells. In vivo injection of anti-PD-L1 antibody effectively suppressed the metastatic colonization of CT26 cells in Il6-/- but not Il6+/+ mice. Finally, we confirmed that colorectal cancer patients with low IL-6 levels in their primary tumors showed prolonged disease-free survival. These findings suggest IL-6 may be a promising target for the treatment of metastasis in colorectal cancers by improving host immunity.
Type: article (author version)
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 北村 秀光

Export metadata:

OAI-PMH ( junii2 , jpcoar )

MathJax is now OFF:


 - Hokkaido University