{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lang Y"],"funding":["Guangdong Provincial Natural Science Foundation","National Natural Science Foundation of China"],"pagination":["110205"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11269928"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["27(7)"],"pubmed_abstract":["Monoacylglycerol acyltransferase-2 (MOGAT2), encodes MOGAT enzyme in the re-synthesis of triacylglycerol and protects from metabolism disorders. While, its precise involvement in colorectal cancer (CRC) progression remains inadequately understood. Our study demonstrated that knockout of Mogat2 in Apc<sup>min/+</sup> mice expedited intestinal tumor growth and progression, indicating that Mogat2 plays a tumor-suppressing role in CRC. Mechanically, Mogat2 deletion resulted in a significant alter the gut microbiota, while Fecal Microbiota Transplantation (FMT) experiments demonstrated that the gut microbiota in Mogat2 deleted mice promoted tumor growth. Furthermore, we identified Mogat2 as a functional regulator suppressing CRC cell proliferation and tumor growth by inhibiting the NF-κB signal"],"journal":["iScience"],"pubmed_title":["Monoacylglycerol acyltransferase-2 inhibits colorectal carcinogenesis in APC<sup>min+/-</sup> mice."],"pmcid":["PMC11269928"],"funding_grant_id":["81972301","KY013915","81902473","2024A1515012800","82073220","82172815"],"pubmed_authors":["Qiu J","Zhong C","Qian C","Ding L","Niu Y","Guo L","Liu Z","Zuo D","Chen X","Li B","Lang Y","Huang B","Yuan Y"],"additional_accession":[]},"is_claimable":false,"name":"Monoacylglycerol acyltransferase-2 inhibits colorectal carcinogenesis in APC<sup>min+/-</sup> mice.","description":"Monoacylglycerol acyltransferase-2 (MOGAT2), encodes MOGAT enzyme in the re-synthesis of triacylglycerol and protects from metabolism disorders. While, its precise involvement in colorectal cancer (CRC) progression remains inadequately understood. Our study demonstrated that knockout of Mogat2 in Apc<sup>min/+</sup> mice expedited intestinal tumor growth and progression, indicating that Mogat2 plays a tumor-suppressing role in CRC. Mechanically, Mogat2 deletion resulted in a significant alter the gut microbiota, while Fecal Microbiota Transplantation (FMT) experiments demonstrated that the gut microbiota in Mogat2 deleted mice promoted tumor growth. Furthermore, we identified Mogat2 as a functional regulator suppressing CRC cell proliferation and tumor growth by inhibiting the NF-κB signal","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul","modification":"2026-03-27T16:51:23.858Z","creation":"2025-08-27T03:11:14.304Z"},"accession":"S-EPMC11269928","cross_references":{"pubmed":["39055928"],"doi":["10.1016/j.isci.2024.110205"]}}