expression was elevated in OSCC cells and tissues compared to normal tissues.
Semaglutide inhibited the proliferation, migration, and invasion of OSCC cells.
The treatment promoted apoptosis in OSCC cells.
Semaglutide activated the while having no significant effect on ERK1/2 or SAPK/JNK.
The pro-apoptotic effects of Semaglutide in OSCC cells are associated with P38 pathway activation.
In vivo experiments confirmed the inhibitory effect of Semaglutide on OSCC tumors in mice.
Simplified
AIMS: Researches have shown that diabetes mellitus (DM) can promote the risk and progression of oral squamous cell carcinoma (OSCC). Semaglutide, a glucagon-like peptide-1 receptor agonist, is currently employed to treat type 2 diabetes mellitus (T2DM) and obesity. This study intends to explore the potential effects and mechanism of Semaglutide on OSCC.
METHODS: The expression of in OSCC cells and tissues was evaluated by qRT-PCR, western blot and immunohistochemistry assays. Cell proliferation, invasion, migration and apoptosis abilities were determined by relevant experiments. Western blot was employed to verify the expression of relevant proteins and examine the effect of Semaglutide on the MAPK signaling pathway. The xenograft transplantation model of OSCC was established to examine the anti-cancer effects of Semaglutide in vivo and immunohistochemistry assays were performed on tumor tissues.
RESULTS: GLP-1R expression was elevated in OSCC cells and tissues as compared with that in normal. Semaglutide effectively inhibited the proliferation, migration and invasion of OSCC cells while concurrently promoting apoptosis. Moreover, Semaglutide specifically activated the without significant influence on ERK1/2 or SAPK/JNK, and its pro-apoptotic effects in OSCC cells was related to P38 pathway activation. Animal experiments verified the inhibitory effect of Semaglutide on OSCC tumors in mice.
CONCLUSIONS: Semaglutide exerts inhibitory actions on OSCC and may induce apoptosis in OSCC cells via the P38 MAPK signaling pathway. This study has significant implications for the treatment of patients with diabetes who are also afflicted by OSCC.
Key numbers
higher in OSCC tissues compared to normal
Expression Increase
Comparison of expression levels in OSCC vs. normal tissues
dose-dependent reduction with Semaglutide treatment
Inhibition of OSCC Cell Proliferation
Effects of Semaglutide on OSCC cell proliferation rates
smaller tumor volume in Semaglutide group vs. control
Tumor Growth Inhibition
Comparison of tumor volumes in treated vs. untreated mice
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