Effect of DNA aptamer through blocking of negative regulation of Wnt/β-catenin signaling in human hair follicle dermal papilla cells

Background: When Wnt binds to the N-terminal of Frizzled, a conformational change occurs in theC-terminal of Frizzled, which binds to Dishevelled1 (Dvl1), aWnt signaling component protein. When Dvl1 binds to the C-terminal of Frizzled, the concentration of beta-catenin increases and it enters the nucleus to transmit cell proliferation signals. CXXC-type zinc finger protein 5 (CXXC5) binds to the Frizzled binding site of Dvl1 and interferes with Dvl1-Frizzled binding. Therefore, blocking CXXC5-Dvl1 binding may induceWnt signal transduction. Materials and methods: We used WD-aptamer, a DNA aptamer that specifically binds to Dvl1 and interferes with CXXC5-Dvl1 interaction. We confirmed the penetration of WD-aptamer into human hair follicle dermal papilla cells (HFDPCs) and measured beta-catenin expression following treatment with WD-aptamer in HFDPCs, wherein Wnt signaling was activated by Wnt3a. In addition, MTTassay was performed to investigate the effect of WD-aptamer on cell proliferation. Results: WD-aptamer penetrated the cell, affected Wnt signaling, and increased beta-catenin expression, which plays an important role in signaling. Additionally, WD-aptamer induced HFDPC proliferation. Conclusion: CXXC5-associated negative feedback of Wnt/beta-catenin signaling can be regulated by interfering with CXXC5-Dvl1 interaction.