Abstract
Background: Angelicin has been reported to have antitumor effects on many cancers. However, few studies on angelicin in oral squamous cell carcinoma (OSCC) have been performed. Methods: In this study, we performed a cell cycle and apoptosis assay, wound healing assay, and transwell assay to assess the effects of angelicin on malignant phenotypes of OSCC in vitro. To determine the potential regulatory mechanism, we conducted differentially expressed genes analysis of OSCC cells. Subsequently, nude mouse xenograft models were used to evaluate the function of angelicin and validate the regulatory mechanism in vivo. Results: The results showed that angelicin inhibited the malignant phenotype of OSCC in vitro and reduced tumor formation in vivo. Mechanistically, angelicin induced the downregulation of the significantly different gene—dual-specificity phosphatase 6 (DUSP6) and the downstream transcription factor c-MYC in the mitogen-activated protein kinase (MAPK) signaling pathway. Conclusion: Our results indicate that angelicin has antitumor effects on OSCC by negatively regulating the DUSP6-mediated cMYC-MAPK signaling pathway and is a promising antitumor drug in OSCC therapy.
Receptor tyrosine kinase, RON, promotes tumor progression by regulating EMT and the MAPK signaling pathway in human oral squamous cell carcinoma
