Background
Oral squamous cell carcinoma (OSCC) is one of the most common cancers, with high metastasis and mortality. Licochalcone A (LCA) is a chalconoid from the root of Glycyrrhiza inflata, which has anti-tumor, anti-inflammatory, anti-angiogenesis effects in many cancers. However, the mechanism that underlies LCA regulating cell proliferation, migration, and invasion in OSCC remains poorly understood.
Conclusions
LCA might inhibit cell proliferation, migration, and invasion through regulating the PI3K/AKT pathway in OSCC, developing a potential chemotherapeutic agent for OSCC.
Methods
LY294002 or insulin-like growth factor 1 (IGF-1) were used to block or stimulate the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) pathway in OSCC cells. Cell proliferation was investigated by MTT assay and proliferating cell nuclear antigen (PCNA) protein level using Western blot. The expression of metastasis-related protein was detected via Western blot. Cell migration and invasion abilities were evaluated by trans-well assay. A murine xenograft model of OSCC was established to investigate the anti-tumor effect of LCA in vivo.
Results
Treatment of LCA inhibited cell proliferation in SCC4 and CAL-27 cells. Moreover, PI3K/AKT signaling was blocked by LY294002, and activated by IGF-1. LCA could suppress proliferation, migration, and invasion of OSCC cells, which was similar to the treatment of LY294002. In addition, LCA decreased IGF-1-induced OSCC progression. In a murine xenograft model, LCA treatment protected against tumor growth and metastasis in vivo. Conclusions: LCA might inhibit cell proliferation, migration, and invasion through regulating the PI3K/AKT pathway in OSCC, developing a potential chemotherapeutic agent for OSCC.