Obovatol inhibits the growth and aggressiveness of tongue squamous cell carcinoma through regulation of the EGF‑mediated JAK‑STAT signaling pathway.

Abstract

Migration and invasion are the most important characteristics of human malignancies which limit cancer drug therapies in the clinic. Tongue squamous cell carcinoma (TSCC) is one of the rarest types of cancer, although it is characterized by a higher incidence, rapid growth and greater potential for metastasis compared with other oral neoplasms worldwide. Studies have demonstrated that the phenolic compound obovatol exhibits anti‑tumor effects. However, the potential mechanisms underlying obovatol‑mediated signaling pathways have not been completely elucidated in TSCC. The present study investigated the anti‑tumor effects and potential molecular mechanisms mediated by obovatol in TSCC cells and tissues. The results of the present study demonstrated that obovatol exerted cytotoxicity in SCC9 TSCC cells, and inhibited their migration and invasion. In addition, obovatol induced apoptosis in SCC9 TSCC cells by increasing caspase 9/3 and apoptotic protease enhancing factor 1 expression levels. Western blot analysis demonstrated that obovatol inhibited the expression of pro‑epidermal growth factor (EGF), Janus kinase (JAK), and signal transducer and activator of transcription (STAT) in SCC9 TSCC cells. A study of the molecular mechanisms demonstrated that depletion of EGF reversed the obovatol‑mediated inhibition of SCC9 TSCC cell growth and aggressiveness. Animal experiments indicated that obovatol significantly inhibited TSCC tumor growth and increased the number of apoptotic cells in tumor tissues. In conclusion, the results of the present study provided scientific evidence that obovatol inhibited TSCC cell growth and aggressiveness through the EGF‑mediated JAK‑STAT signaling pathway, suggesting that obovatol may be a potential anti‑TSCC agent.