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Int. J. Mol. Sci. 2016, 17(5), 643; doi:10.3390/ijms17050643

The Role of Chemokines in Promoting Colorectal Cancer Invasion/Metastasis

1
Department of Surgery, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan
2
Moores Cancer Center, University of California, San Diego, CA 92093, USA
3
Department of Pharmacology, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan
*
Author to whom correspondence should be addressed.
Academic Editor: Li Yang
Received: 30 March 2016 / Revised: 18 April 2016 / Accepted: 25 April 2016 / Published: 28 April 2016
(This article belongs to the Special Issue Tumor Microenvironment and Metabolism)
View Full-Text   |   Download PDF [1135 KB, uploaded 28 April 2016]   |  

Abstract

Colorectal cancer (CRC) is one of the leading causes of cancer-related death worldwide. Although most of the primary CRC can be removed by surgical resection, advanced tumors sometimes show recurrences in distant organs such as the liver, lung, lymph node, bone or peritoneum even after complete resection of the primary tumors. In these advanced and metastatic CRC, it is the tumor-stroma interaction in the tumor microenvironment that often promotes cancer invasion and/or metastasis through chemokine signaling. The tumor microenvironment contains numerous host cells that may suppress or promote cancer aggressiveness. Several types of host-derived myeloid cells reside in the tumor microenvironment, and the recruitment of them is under the control of chemokine signaling. In this review, we focus on the functions of chemokine signaling that may affect tumor immunity by recruiting several types of bone marrow-derived cells (BMDC) to the tumor microenvironment of CRC. View Full-Text
Keywords: colon cancer; tumor microenvironment; myeloid cells; cancer immunity colon cancer; tumor microenvironment; myeloid cells; cancer immunity
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Itatani, Y.; Kawada, K.; Inamoto, S.; Yamamoto, T.; Ogawa, R.; Taketo, M.M.; Sakai, Y. The Role of Chemokines in Promoting Colorectal Cancer Invasion/Metastasis. Int. J. Mol. Sci. 2016, 17, 643.

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