A Novel N-Sulfonylamidine-Based Derivative Inhibits Proliferation, Migration, and Invasion in Human Colorectal Cancer Cells by Suppressing Wnt/β-Catenin Signaling Pathway

Wnt signaling has been implicated in the development and metastasis of colorectal cancer (CRC), as well as poorer outcomes. Thus, targeting the Wnt/beta-catenin signaling pathway is expected to be a promising treatment option for the therapy of advanced metastatic CRC. A new N-sulfonylamidine derivative (26ag) has been confirmed to suppress the growth of tumor cells by inhibiting C-met, showing strong anti-cancer activity. In this paper, we test the effectiveness of 26ag in suppressing CRC cell proliferation, invasion, and migration. In this regard, 26ag decreased the mRNA and protein expressions of important hallmarks associated with epithelial to mesenchymal transition (EMT). Furthermore, we provide evidence that beta-catenin-dependent signaling is involved in 26ag-induced Wnt/beta-catenin pathway effects in CRC, using in vitro cell culture and computer docking models. Our study indicates that inhibition of Wnt/beta-catenin by a novel compound, 26ag, demonstrates possibility for drug development in the therapy of CRC.

Automated summary

The study investigated a novel N-sulfonylamidine derivative 26ag in suppressing CRC cell proliferation and migration, revealing its strong anti-cancer activity by inhibiting C-met and reducing expression of hallmarks associated with EMT, involving the β-catenin-dependent pathway. This research demonstrates the potential of 26ag as a promising drug candidate for the therapy of CRC by inhibiting the Wnt/β-catenin pathway.