Delineating the pathophysiological role of Dectin-1 in colorectal tumorigenesis based on murine and clinical studies (IMAGE)

Tokyo University of Science

Delineating the pathophysiological role of Dectin-1 in colorectal tumorigenesis based on murine and clinical studies

Caption

Mouse model of familial colorectal adenomatosis (ApcMin) showing significantly fewer colonic polyps in Dectin-1-deficient (Clec7a–/–) mice; B. Polyps show reduced expression of PGE2 synthase (Cox2). In vitro, Cox2 expression is induced in myeloid cells by curdlan—a high-molecular-weight β-glucan—and conversely inhibited by laminarin—a low-molecular-weight β-glucan; C. Increased IL-22BP expression in Clec7a–/– mice; D. Dectin-1 gene loss increases the lifespan of ApcMin mice, whereas deletion of the IL-22BP gene results in a shorter lifespan; E. The number of myeloid-derived suppressor cells (MDSCs) is reduced in Clec7a–/– mice; F. Dietary laminarin reduces the number of AOM-DSS-induced colon polyps G. Among colorectal cancer patients, those with high dectin-1 expression have significantly lower survival rates than those with low dectin-1 expression; H. Dectin-1 expression in colorectal cancer patients correlates with cancer severity.

Credit

Yoichiro Iwakura from Tokyo University of Science Image Source Link: https://www.nature.com/articles/s41467-023-37229-x

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