Salivary gland adenoid cystic carcinoma (SACC) is one of the most common malignancies in the oral and maxillofacial region. Carcinoma-associated fibroblast (CAF) is an important component in the tumor microenvironment and participates in SACC progression. In this study, we established a CAF cell line derived from a human SACC and named it CAF-SA. It was identified that CAF-SA expressed typical CAF biomarkers. Then, we studied the cellular communications between CAF-SA, tumor cells and endothelial cells. It was found that CAF-SA promoted the migration, invasion, and proliferation of SACC tumor cells in vitro. In addition, tube formation by endothelial cells was enhanced by CAF-SA. In vivo experiment showed that SACC cells formed larger xenografts in nude mice when they were transplanted with CAF-SA. Overall, we demonstrated that CAF-SA exhibited the most important defining feature of CAF by promoting cancer progression.
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.
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