Abstract

Tongue cancer represents a prevalent malignant tumor within the oral and maxillofacial region. The purpose of this study was to clarify the molecular mechanisms underlying Schisandrin A involvement in tongue cancer. The viability and proliferation of tongue cancer cells were evaluated through modulation transfer spectroscopy and clone formation assays. Scratch and Transwell tests were used to investigate migration and invasion capabilities. The Wnt/beta-catenin signaling pathway-related proteins were investigated employing Western blot analysis. The tumorigenic potential of tongue cancer was assessed using a xenograft assay in the presence of Schisandrin A. To further substantiate the impact of Schisandrin A on tongue cancer, lithium chloride treatment was administered, and the effects were validated in tongue cancer xenograft models, researching the Wnt/beta-catenin signaling pathway’s role in particular. In a dose-dependent manner, Schisandrin A exhibited a notable inhibitory effect on the viability, proliferation, migration, and invasive potential of tongue cancer cells (p<0.05). In tongue cancer cells, Schisandrin A efficiently downregulated proteins associated to the Wnt/beta-catenin signaling pathway (p<0.05). Furthermore, in vivo tests demonstrated that Schisandrin A down-regulated the proteins associated with this signaling pathway in the tumor in addition to preventing tongue cancer tumor growth (p<0.05). The inhibitory influence of Schisandrin A on tongue cancer was partially counteracted by lithium chloride. Schisandrin A successfully inhibited the formation of tumors in tongue cancer as well as the spread and multiplication of tongue cancer cells. The Wnt/beta-catenin signaling pathway was downregulated to produce this inhibitory effect. The findings of this investigation shed light on Schisandrin A function and potential mechanism in addressing tongue cancer and provide a novel reference for its treatment.