Bibliographic Details
| Title: |
Semaglutide, a glucagon-like peptide-1 receptor agonist, inhibits oral squamous cell carcinoma growth through P38 MAPK signaling pathway |
| Authors: |
Can Wang, Zhengzheng Wu, Jiaying Zhou, Bin Cheng, Yulei Huang |
| Source: |
Journal of Cancer Research and Clinical Oncology, Vol 151, Iss 3, Pp 1-15 (2025) |
| Publisher Information: |
Springer, 2025. |
| Publication Year: |
2025 |
| Collection: |
LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens |
| Subject Terms: |
GLP-1R, Semaglutide, OSCC, P38 MAPK signaling pathway, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282 |
| More Details: |
Abstract 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 GLP-1R 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 P38 MAPK signaling pathway 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. |
| Document Type: |
article |
| File Description: |
electronic resource |
| Language: |
English |
| ISSN: |
1432-1335 |
| Relation: |
https://doaj.org/toc/1432-1335 |
| DOI: |
10.1007/s00432-025-06154-5 |
| Access URL: |
https://doaj.org/article/7ba3441ea30449658bac7b0cdd1ee600 |
| Accession Number: |
edsdoj.7ba3441ea30449658bac7b0cdd1ee600 |
| Database: |
Directory of Open Access Journals |
Full Text from SpringerLink