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 the C‐terminal of Frizzled, which binds to Dishevelled1 (Dvl1), a Wnt signaling component protein. When Dvl1 binds to the C‐terminal of Frizzled, the concentration of β‐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 induce Wnt 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 β‐catenin expression following treatment with WD‐aptamer in HFDPCs, wherein Wnt signaling was activated by Wnt3a. In addition, MTT assay was performed to investigate the effect of WD‐aptamer on cell proliferation. RESULTS: WD‐aptamer penetrated the cell, affected Wnt signaling, and increased β‐catenin expression, which plays an important role in signaling. Additionally, WD‐aptamer induced HFDPC proliferation. CONCLUSION: CXXC5‐associated negative feedback of Wnt/β‐catenin signaling can be regulated by interfering with CXXC5–Dvl1 interaction.