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Alterations in Wnt signaling in folate deficient cells

Folate is an essential dietary vitamin involved in methylation reactions. Insufficient dietary folate has been associated with various developmental and adult diseases such as neural tube defects and colorectal cancer. The basis for this association has not been clearly defined. The Wnt signaling pathway has multiple functions, affecting cell growth, differentiation, and development. The purpose of this study was to determine if folate deficiency leads to altered Wnt signaling with a focus on β‐catenin activity, protein levels, and cellular localization. NIH3T3 cells containing the TOPFlash β‐catenin luciferase reporter were grown for 4, 8, and 10 days in folate deficient and sufficient custom DMEM medium and treated, with and without a Wnt3a conditioned medium, to activate the Wnt pathway. β‐catenin activity as measured by luciferase activity per unit DNA was higher in folate deficient cells at 8 and 10 days in stimulated cells. β‐catenin protein levels as assayed by Western blot analysis were slightly higher in stimulated folate deficient cells at 10 days. Localization of β‐catenin by immunofluorescence indicated increased nuclear localization of β‐catenin in folate deficient cells of both Wnt3a stimulated and unstimulated cells at 10 days. Overall, these results suggest that folate deficiency may lead to altered cell function, in part, due to changes in Wnt signaling. Research Support: NIH R15 DK070581