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• W2891497601 abstract "Signal transducer and activator of transcription 1 (STAT1) is part of the Janus kinase (JAK/STAT) signaling pathway that controls critical events in intestinal immune function related to innate and adaptive immunity. Recent studies have implicated STAT1 in tumor⁻stroma interactions, and its expression and activity are perturbed during colon cancer. However, the role of STAT1 during the initiation of inflammation-associated cancer is not clearly understood. To determine the role of STAT1 in colitis-associated colorectal cancer (CAC), we analyzed the tumor development and kinetics of cell recruitment in wild-type WT or STAT1-/- mice treated with azoxymethane (AOM) and dextran sodium sulfate (DSS). Following CAC induction, STAT1-/- mice displayed an accelerated appearance of inflammation and tumor formation, and increased damage and scores on the disease activity index (DAI) as early as 20 days after AOM-DSS exposure compared to their WT counterparts. STAT1-/- mice showed elevated colonic epithelial cell proliferation in early stages of injury-induced tumor formation and decreased apoptosis in advanced tumors with over-expression of the anti-apoptotic protein Bcl2 at the colon. STAT1-/- mice showed increased accumulation of Ly6G⁺Ly6C-CD11b⁺ cells in the spleen at 20 days of CAC development with concomitant increases in the production of IL-17A, IL-17F, and IL-22 cytokines compared to WT mice. Our findings suggest that STAT1 plays a role as a tumor suppressor molecule in inflammation-associated carcinogenesis, particularly during the very early stages of CAC initiation, modulating immune responses as well as controlling mechanisms such as apoptosis and cell proliferation." @default.
• W2891497601 created "2018-09-27" @default.
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• W2891497601 date "2018-09-19" @default.
• W2891497601 modified "2023-10-17" @default.
• W2891497601 title "Deficiency in STAT1 Signaling Predisposes Gut Inflammation and Prompts Colorectal Cancer Development" @default.
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• W2891497601 doi "https://doi.org/10.3390/cancers10090341" @default.
• W2891497601 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6162416" @default.
• W2891497601 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30235866" @default.
• W2891497601 hasPublicationYear "2018" @default.
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