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Deciphering How Nutrition Drives Colitis-associated Colorectal Carcinogenesis
Targeted nutritional intervention for cancer entities is a promising approach that still is in its infancies. Hence, there is a strong need to identify molecular targets within the cellular metabolic framework of cancer cells. Mucosal energy metabolism is pivotal for intestinal barrier homeostasis and is highly modulated by western diet-related chronic inflammation.
On our way to better understand modulation of mucosal metabolism in the context of colorectal carcinogenesis, we recently iden¬tified a complete new molecular mechanism that describes how intestinal inflammation induces a metabolic switch and thereby boosts tumor cell proliferation. Of note, this mechanism directly links in- flammatory processes to colorectal carcinogenesis and can be therapeutically inhibited by targeted nutritional interventions as recently demonstrated in yet unpublished experimental mouse studies by our group (Fig. 1).
The aim of the project funded by the Erich and Gertrud Roggenbuck Foundation is to gain deeper insights into how nutrition decisively promotes intestinal inflammation (= Nutri-Inflammation) and thus colorectal carcinogenesis. Based on these findings, we will develop novel nutrition-based targeted strategies to prevent colitis-driven CRC.