ArticleJournal of Cancer2024
Imatinib inhibits oral squamous cell carcinoma by suppressing the PI3K/AKT/mTOR signaling pathway.
Article in Journal of Cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Sweet apple e-cigarette vapor differentially modulates the mTOR pathway in oral squamous cell carcinoma cell lines.Frontiers in oncology · 2026Article
- Vemurafenib Induces Apoptosis via JNK Activation and AKT Inhibition in Hepatocellular Carcinoma.Journal of Cancer · 2026Article
- Radiation-Induced Fibrosis (RIF) in Head and Neck Squamous Cell Carcinoma (HNSCC): A Review.Cells · 2025Review
- Design and biological evaluation of peptide disruptors targeting YAP1-TEAD interaction for oral cancer.BMC oral health · 2025Article
- Article
- Novel receptor tyrosine kinase-targeted strategies to overcome resistance in oral squamous cell carcinoma.Pharmacological reports : PR · 2025Review
- Synergistic inhibition of proliferation and induction of apoptosis in oral tongue squamous cell carcinoma by mebendazole and paclitaxel via PI3K/AKT pathway mitigation.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Elucidating the role of lipid metabolism dysregulation in the transition from oral lichen planus to oral squamous cell carcinoma.Journal of translational medicine · 2025Article
- Dysregulated PI3K/AKT signaling in oral squamous cell carcinoma: The tumor microenvironment and epigenetic modifiers as key drivers.Oncology research · 2025Review
- Evolving Therapeutic Strategies in Esophageal Squamous Cell Carcinoma: Advances and Perspectives.Journal of cancer prevention · 2024Review
- Advances in Preventive and Therapeutic Strategies for Oral Cancer: A Short Review.Journal of cancer prevention · 2024Review
- Parishin A Inhibits Oral Squamous Cell Carcinoma via the AKT/mTOR Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2024Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oral squamous cell carcinoma (OSCC) is a prevalent oral and maxillofacial cancer with high mortality as OSCC cells readily invade tissues and metastasize to cervical lymph nodes. Although imatinib exhibits potential anticancer and remarkable clinical activities that therapeutically affect several cancer types, its specific impact on OSCC has yet to be fully explored. Therefore, this study investigated the potential anticancer effect of imatinib on OSCC cells and the underlying mechanisms. The Cell Counting Kit-8 was used to determine the impact of imatinib on cell viability. Then, morphological cell proliferation analysis was conducted to examine how imatinib impacted OSCC cell growth. Moreover, OSCC cell migration was determined through wound-healing assays, and colony formation abilities were investigated through the soft agar assay. Lastly, the effect of imatinib on OSCC cell apoptosis was verified with flow cytometry, and its inhibitory mechanism was confirmed through Western blot. Our results demonstrate that imatinib effectively inhibited OSCC cell proliferation and significantly curtailed OSCC cell viability in a time- and concentration-dependent manner. Furthermore, imatinib suppressed migration and colony formation while promoting OSCC cell apoptosis by enhancing p53, Bax, and PARP expression levels and reducing Bcl-2 expression. Imatinib also inhibited the PI3K/AKT/mTOR signaling pathway and induced OSCC cell apoptosis, demonstrating the potential of imatinib as a treatment for oral cancer.
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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 OpenQuestion graph.