<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lang Y</submitter><funding>Guangdong Provincial Natural Science Foundation</funding><funding>National Natural Science Foundation of China</funding><pagination>110205</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11269928</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>27(7)</volume><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&lt;sup>min/+&lt;/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</pubmed_abstract><journal>iScience</journal><pubmed_title>Monoacylglycerol acyltransferase-2 inhibits colorectal carcinogenesis in APC&lt;sup>min+/-&lt;/sup> mice.</pubmed_title><pmcid>PMC11269928</pmcid><funding_grant_id>81972301</funding_grant_id><funding_grant_id>KY013915</funding_grant_id><funding_grant_id>81902473</funding_grant_id><funding_grant_id>2024A1515012800</funding_grant_id><funding_grant_id>82073220</funding_grant_id><funding_grant_id>82172815</funding_grant_id><pubmed_authors>Qiu J</pubmed_authors><pubmed_authors>Zhong C</pubmed_authors><pubmed_authors>Qian C</pubmed_authors><pubmed_authors>Ding L</pubmed_authors><pubmed_authors>Niu Y</pubmed_authors><pubmed_authors>Guo L</pubmed_authors><pubmed_authors>Liu Z</pubmed_authors><pubmed_authors>Zuo D</pubmed_authors><pubmed_authors>Chen X</pubmed_authors><pubmed_authors>Li B</pubmed_authors><pubmed_authors>Lang Y</pubmed_authors><pubmed_authors>Huang B</pubmed_authors><pubmed_authors>Yuan Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Monoacylglycerol acyltransferase-2 inhibits colorectal carcinogenesis in APC&lt;sup>min+/-&lt;/sup> mice.</name><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&lt;sup>min/+&lt;/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</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jul</publication><modification>2026-03-27T16:51:23.858Z</modification><creation>2025-08-27T03:11:14.304Z</creation></dates><accession>S-EPMC11269928</accession><cross_references><pubmed>39055928</pubmed><doi>10.1016/j.isci.2024.110205</doi></cross_references></HashMap>