Published online Jan 14, 2016. doi: 10.3748/wjg.v22.i2.833
Peer-review started: March 30, 2015
First decision: June 25, 2015
Revised: July 17, 2015
Accepted: November 9, 2015
Article in press: November 9, 2015
Published online: January 14, 2016
Processing time: 284 Days and 21 Hours
Chemokines belong to a superfamily of small, cytokine-like proteins, which induce multiple physiological functions, particularly cytoskeletal rearrangement and compartment-specific migration through their interaction with G-protein-coupled receptors. Chemokines and their receptors have been widely acknowledged as essential and selective mediators in leukocyte migration in inflammatory response. It is now established that the chemokine/chemokine receptor system is also used by cancer cells to direct lymphatic and haematogenous spreading and additionally has an impact on the site of metastatic growth of different tumours. In recent years an increasing number of studies have drawn attention to CC-chemokine cysteine motif chemokine ligand 20 (CCL20) and its physiological sole receptor CCR6 to play a role in the onset, development and metastatic spread of various gastrointestinal cancer entities. Among various cancer types CCR6 was also demonstrated to be significantly overexpressed in colorectal cancer (CRC) and stimulation by its physiological ligand CCL20 has been reported to promote CRC cell proliferation and migration in vitro. Further, the CCL20/CCR6 system apparently plays a role in the organ-selective liver metastasis of CRC. Here we review the literature on expression patterns of CCL20 and CCR6 and their physiological interactions as well as the currently presumed role of CCL20 and CCR6 in the formation of CRC and the development of liver metastasis, providing a potential basis for novel treatment strategies.
Core tip: Here we review the current literature published with respect to the expression pattern of chemokine/chemokine receptor pair cysteine motif chemokine ligand 20 (CCL20)/CCR6 and their physiological interactions as well as the currently presumed role of the CCL20/CCR6 system in the onset and development of colorectal cancer (CRC) and its apparent role in the organ-selective metastatic spread of CRC cells to the liver. Disrupting the chemokine/chemokine receptor interaction of CCL20/CCR6 may therefore be a promising novel treatment strategy in CRC and metastasis.