ArticleJournal of cancer research and clinical oncology2025
Semaglutide, a glucagon-like peptide-1 receptor agonist, inhibits oral squamous cell carcinoma growth through P38 MAPK signaling pathway.
Article in Journal of cancer research and clinical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Cancer outcomes and biological mechanisms among patients with type 2 diabetes mellitus using glucagon-like peptide-1 receptor agonists: a systematic review and meta-analysis.Frontiers in oncology · 2026Pooled it
- Role of GLP-1 receptor agonists in the prevention and treatment of obesity-related cancer.Internal and emergency medicine · 2026Review
- Insulin Resistance as a Systemic Metabolic Risk State for Cancer: Mechanisms, Biomarkers, and Prevention.International journal of molecular sciences · 2026Review
- The Multifaceted Nature of GLP-1: Molecular Mechanisms and Signaling Pathways in Metabolic and Neurodegenerative Diseases.International journal of molecular sciences · 2026Review
- Incretin Mimetics in Cancer and Cardiovascular Disease: JACC: CardioOncology State-of-the-Art Review.JACC. CardioOncology · 2026Review
- In silico evaluation of anticancer peptide as a novel therapeutic agent against AURKA for targeting oral carcinogenesis.Journal of molecular modeling · 2025Article
- Interconnected Mechanistic Pathways, Molecular Biomarkers, and Therapeutic Approach of Oral Cancer in Patients with Diabetes Mellitus.Current issues in molecular biology · 2025Review
- GLP-1 receptor agonists in the context of cancer: the road ahead.American journal of physiology. Cell physiology · 2025 · on this mapReview
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsResearches 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.
methodsThe 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.
resultsGLP-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.
conclusionsSemaglutide 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.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.