According to the Centers for Disease Control and Prevention (CDC), colorectal cancer is the second leading cause of cancer death in the United States. Researchers have observed elevated levels of the macrophage inflammatory protein CCL20 in colorectal cancer. Interactions between CCL20 and its receptor, CCR6, promote colorectal cancer through effects on neoplastic epithelial cells and modulation of the tumor microenvironment. However, the mechanism of these effects are not yet fully understood.
“In particular, CCL20 acting on CCR6 expressed by colorectal cancer neoplastic epithelial cells induces proliferation, migration, and initiates an auto-feedback loop by inducing further secretion of CCL20. The mechanisms through which CCL20-CCR6 interactions elicit these effects is poorly understood.”
Researchers—from the VA Boston Healthcare System, Harvard Medical School, Beth Israel Deaconess Medical Center, Dana-Farber Cancer Institute, and Brigham and Women’s Hospital—conducted a study investigating the signaling pathways and mechanisms that underlie this colorectal cancer-promoting molecule. In 2021, the team authored a research paper, which was chosen as the cover paper of Oncotarget’s Volume 12, Issue 24, and entitled, “CCL20 induces colorectal cancer neoplastic epithelial cell proliferation, migration, and further CCL20 production through autocrine HGF-c-Met and MSP-MSPR signaling pathways."
Full blog - https://www.oncotarget.org/2021/11/24/new-study-investigation-of-colorectal-cancer-promoting-protein/
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DOI - https://doi.org/10.18632/oncotarget.28131
Full text - https://www.oncotarget.com/article/28131/text/
Correspondence to - Jason S. Gold - jgold@bwh.harvard.edu
Keywords - CCL20, CCR6, HGF, MSP, colorectal cancer
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