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• W2000925949 abstract "The Ron receptor tyrosine kinase is overexpressed in approximately half of all human colon cancers. Increased Ron expression positively correlates with tumor progression, and reduction of Ron levels in human colon adenocarcinoma cells reverses their tumorigenic properties. Nearly all colon tumors demonstrate loss of the adenomatous polyposis coli (APC) tumor suppressor, an early initiating event, subsequently leading to β-catenin stabilization. To understand the role of Ron in early stage intestinal tumorigenesis, we generated Apc-mutant (ApcMin/+) mice with and without Ron signaling. Interestingly, we report here that significantly more ApcMin/+ Ron-deficient mice developed higher tumor burden than ApcMin/+ mice with wild-type Ron. Even though baseline levels of intestinal crypt proliferation were increased in the ApcMin/+ Ron-deficient mice, loss of Ron did not influence tumor size or histological appearance of the ApcMin/+ adenomas, nor was β-catenin localization changed compared to ApcMin/+ mice with Ron. Together, these data suggest that Ron may be important in normal intestinal tissue homeostasis, but that the expression of this receptor is not required for the formation and growth of adenomas in ApcMin/+ mice. © 2009 Wiley-Liss, Inc." @default.
• W2000925949 created "2016-06-24" @default.
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• W2000925949 date "2009-05-18" @default.
• W2000925949 modified "2023-09-26" @default.
• W2000925949 title "The Ron receptor tyrosine kinase is not required for adenoma formation in Apc Min/+ mice" @default.
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• W2000925949 doi "https://doi.org/10.1002/mc.20551" @default.
• W2000925949 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4102426" @default.
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