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• W1964592237 abstract "Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DCInorganic phosphate is a common dietary element that is critical to the human body on many levels however the effects of changes in serum phosphate on cell and tissue behavior are not well understood. Due, in part, to the increased consumption of processed foods, the amount of inorganic phosphate in the American diet continues to rise above levels already considered high by the FDA. There is a growing appreciation that changes in serum phosphate levels influence pathological states associated with aging such as cancer, bone metabolism, and cardiovascular function, even in individuals with normal renal function. The causes are only beginning to be elucidated but are likely a combination of endocrine, paracrine, autocrine, and cell autonomous effects. Recent studies in mice have demonstrated that a diet high in phosphate, relative to a reduced phosphate diet, increases tumorigenesis in the two-stage skin carcinogenesis model as well as the Kras lung cancer model. Using cell cultures models we have determined that high phosphate results in increased proliferation and transformation as measured by XTT, cell counts, soft agar and focus formation assays. Our in vitro studies have also identified specific signaling cascades induced by elevated extracellular phosphate which result in the temporal and dynamic regulation of hundreds of phosphate responsive genes. A subset of the Pi-responsive genes including the Forkhead box protein C2 (FOXC2), osteopontin (spp1), Cyr61, and Vegf among others, has been previously linked to stimulation of angiogenesis leading to the hypothesis that conditioned medium from phosphate treated cells would increase angiogenesis. We confirmed the phosphate-induced expression of these genes in a number of cancer cells including breast, colon, and lung. The increased expression of these genes was determined to be dependent on phosphate transport as well as FGF receptor and ERK1/2 signaling. Using human umbilical cord vascular endothelial cells (HUVECs) we determined that, in fact, conditioned medium from these phosphate treated cancer cells increased both migration and tube formation in the HUVEC model. Knockdown of FOXC2 inhibited phosphate induced gene expression in cancer cells as well as eliminating the stimulation of HUVEC migration in response to Pi-treated cancer cell conditioned medium. These results suggest that a cellular environment with elevated phosphate promotes multiple aspects of tumorigenesis including angiogenesis.Citation Format: Yiming Lin, Laura M. Garneys, Kelly E. Bennett, George R. Beck. A high phosphate environment induces angiogenesis, which is mediated by FOXC2. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3894. doi:10.1158/1538-7445.AM2013-3894" @default.
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• W1964592237 date "2013-04-15" @default.
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• W1964592237 title "Abstract 3894: A high phosphate environment induces angiogenesis, which is mediated by FOXC2." @default.
• W1964592237 doi "https://doi.org/10.1158/1538-7445.am2013-3894" @default.
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