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10.1038/s41420-025-02768-3 http://scihub22266oqcxt.onion/10.1038/s41420-025-02768-3 C12533223!12533223 !41102141     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=41102141 &cmd=llinks): Failed to open stream: HTTP request failed! 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Targeting FADS1-mediated lipid metabolism and signaling: a novel therapeutic strategy for precision oncology in colorectal and esophageal cancers |pdf=|usr=}}{{41102141 }} gab.com Text Targeting FADS1-mediated lipid metabolism and signaling: a novel therapeutic strategy for precision oncology in colorectal and esophageal cancers JO: Cell Death Discov http://www.kidney.de/pget.php?&tw=1&pmid=41102141 #FOAvip Gastrointestinal (GI) cancers exhibit aberrant lipid metabolism, yet the causal mechanisms remain elusive. Here, we integrated Mendelian randomization (MR) and multi-omics data to dissect metabolic drivers of 20 GI diseases. Focusing on colorectal (CC) and esophageal cancer (EC), we identified five metabolites (e.g., 1,2-di-palmitoyl-sn-glycero-3-phosphocholine) and arachidonic acid ethyl ester as causal drivers. Summary-data-based MR and colocalization analysis (PP.H4?>?0.75) revealed FADS1 as a master regulator of these metabolites, with genetic variants exhibiting tissue-specific lipidomic effects. Functional validation using FADS1-knockout cell lines and mouse models demonstrated that FADS1 inhibition suppresses tumor cell proliferation, migration, and invasion while promoting apoptosis. In vivo, FADS1 deletion reduced chemically induced CC/EC tumor burden by 62-75%, accompanied by decreased Ki-67/MMP-9 expression and inflammatory infiltration. Mechanistically, FADS1 ablation disrupted lipid metabolism (reduced linoleic acid and arachidonic acid) and attenuated PI3K/AKT and MAPK signaling. Multi-omics integration further corroborated FADS1-mediated epigenetic regulation (e.g., mQTL-driven DNA methylation). This study establishes FADS1 as a pivotal orchestrator of GI carcinogenesis via metabolic reprogramming and signaling dysregulation, offering a compelling therapeutic target for precision oncology in CC and EC. Regulatory mechanisms of FADS1 in CC and EC. Twit Text FOAVip Targeting FADS1-mediated lipid metabolism and signaling: a novel therapeutic strategy for precision oncology in colorectal and esophageal cancers ????Cell Death Discov http://www.kidney.de/pget.php?&tw=1&pmid=41102141 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=41102141 #FOAvip English Wikipedia <ref>{{Cite pmid|41102141 }}</ref> Targeting FADS1-mediated lipid metabolism and signaling: a novel therapeutic strategy for precision oncology in colorectal and esophageal cancers #MMPMID41102141 Lian J ; Duan X ; Chen W ; Zhang X ; Lu M ; Lin Z ; Wu Z ; Ma L ; Liang R Cell Death Discov 2025[Oct]; 11 (1 ): 460 PMID41102141 show ga Gastrointestinal (GI) cancers exhibit aberrant lipid metabolism, yet the causal mechanisms remain elusive. Here, we integrated Mendelian randomization (MR) and multi-omics data to dissect metabolic drivers of 20 GI diseases. Focusing on colorectal (CC) and esophageal cancer (EC), we identified five metabolites (e.g., 1,2-di-palmitoyl-sn-glycero-3-phosphocholine) and arachidonic acid ethyl ester as causal drivers. Summary-data-based MR and colocalization analysis (PP.H4?>?0.75) revealed FADS1 as a master regulator of these metabolites, with genetic variants exhibiting tissue-specific lipidomic effects. Functional validation using FADS1-knockout cell lines and mouse models demonstrated that FADS1 inhibition suppresses tumor cell proliferation, migration, and invasion while promoting apoptosis. In vivo, FADS1 deletion reduced chemically induced CC/EC tumor burden by 62-75%, accompanied by decreased Ki-67/MMP-9 expression and inflammatory infiltration. Mechanistically, FADS1 ablation disrupted lipid metabolism (reduced linoleic acid and arachidonic acid) and attenuated PI3K/AKT and MAPK signaling. Multi-omics integration further corroborated FADS1-mediated epigenetic regulation (e.g., mQTL-driven DNA methylation). This study establishes FADS1 as a pivotal orchestrator of GI carcinogenesis via metabolic reprogramming and signaling dysregulation, offering a compelling therapeutic target for precision oncology in CC and EC. Regulatory mechanisms of FADS1 in CC and EC. äTargeting FADS1-mediated lipid metabolism and signaling: a novel thera(epmc).pdf DeepDyve Pubget Overpricing