LF3 inhibits Wnt/β-catenin signaling in cells with exogenous reporter genes and in colorectal cancer cells with high intrinsic Wnt activity, with IC50 values of 1.65 μM (β-Catenin/TCF4, AlphaScreen) and 1.82 μM (β-Catenin/TCF4, ELISA). LF3 also suppresses cancer cell traits associated with Wnt signaling, including high cell motility, cell cycle progression, and overexpression of Wnt target genes. However, LF3 does not induce cell death or interfere with cadherin-mediated cell adhesion. Notably, the self-renewal capacity of cancer stem cells is blocked by LF3 in a concentration-dependent manner[1].
LF3 动物研究
Animal study
LF3 reduces tumor growth and induces differentiation in a mouse colorectal cancer xenograft model. When mice with GFPhigh cells were treated with LF3 at a dose of 50 mg/kg, there was a significant reduction in tumor growth. LF3 treatment did not disrupt the normal histology of gut of mice[1].
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