Mucin 1 promotes salivary gland cancer cell proliferation and metastasis by regulating the epidermal growth factor receptor signaling pathway

• Main Authors: Hao Lu (Author), Wan-Lin Xu (Author), Yi-Fan Wu (Author), Wen-Jun Yang (Author), Sheng-Wen Liu (Author)
• Format: Book
• Published: Elsevier, 2023-10-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.
• Notes: 1991-7902; 10.1016/j.jds.2023.01.035
• Keywords: EGFR; MUC1; Metastasis; Proliferation; Salivary gland cancer; Dentistry; RK1-715
• Source: Journal of Dental Sciences, Vol 18, Iss 4, Pp 1651-1662 (2023)

Background/purpose: Salivary gland cancer (SGC) is the common malignant tumor of the head and neck region with poor prognosis. Mucin 1 (MUC1) has been reported to be associated with the development of cancer. However, whether MUC1 contributed to the progression of SGC remains to be explored. Materials and methods: Immunohistochemical analysis was used to explore the expression levels of MUC1 in SGC tissues. Cell proliferation, colony formation, wound healing, transwell, and xenograft assays were performed to examine the effects of MUC1 on SGC in vitro and in vivo. Results: We found that the expression level of MUC1 was significantly upregulated in SGC tissues, and the expression level of MUC1 was significantly correlated with lymph node metastasis and TNM stage of SGC. Further exploration demonstrated that MUC1 knockdown drastically inhibited, while its overexpression promoted, cell growth, colony formation, migration, and invasion abilities of SGC cells in vitro. MUC1 knockdown significantly inhibited tumor growth in vivo, and vice versa. More importantly, we found that MUC1 promotes malignant phenotypes of SGC cells by regulating the epidermal growth factor receptor (EGFR) signaling pathway. Conclusion: Our results revealed that MUC1 promotes the development of SGC by mediating the EGFR signaling pathway, which highlights the potential therapeutic target of MUC1/ EGFR in SGC.