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• W2891707166 abstract "Colon cancer is a devastating illness that is associated with gut inflammation. Here, we explored the possible role of lipin-1, a phosphatidic acid phosphatase, in the development of colitis-associated tumorigenesis. Azoxymethane and dextran sodium sulfate-treated (DSS-treated) animals deficient in lipin-1 harbored fewer tumors and carcinomas than WT animals due to decreased cellular proliferation, lower expression of antiapoptotic and protumorigenic factors, and a reduced infiltration of macrophages in colon tumors. They also displayed increased resistance to DSS-induced colitis by producing less proinflammatory cytokines and experiencing less immune infiltration. Lipin-1-deficient macrophages from the colon were less activated and displayed lower phosphatidic acid phosphatase activity than WT macrophages isolated from DSS-treated animals. Transference of WT macrophages into lipin-1-deficient animals was sufficient to increase colitis burden. Furthermore, treatment of lipin-1-deficient mice with IL-23 exacerbated colon inflammation. Analysis of human databases from colon cancer and ulcerative colitis patients showed that lipin-1 expression is increased in those disorders and correlates with the expression of the proinflammatory markers CXCL1 and CXCL2. And finally, clinically, LPIN1 expression had prognostic value in inflammatory and stem-cell subtypes of colon cancers. Collectively, these data demonstrate that lipin-1 is a critical regulator of intestinal inflammation and inflammation-driven colon cancer development." @default.
• W2891707166 created "2018-09-27" @default.
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• W2891707166 date "2018-09-20" @default.
• W2891707166 modified "2023-10-17" @default.
• W2891707166 title "The phosphatidic acid phosphatase lipin-1 facilitates inflammation-driven colon carcinogenesis" @default.
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• W2891707166 doi "https://doi.org/10.1172/jci.insight.97506" @default.
• W2891707166 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6237220" @default.
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• W2891707166 hasPublicationYear "2018" @default.
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