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Semaglutide may slow mouth cancer growth by activating the p38 MAPK cell signaling pathway
Updated
Abstract
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
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