Related Experiment Video
Updated: Jul 5, 2025

Molecular and Immunologic Techniques in a Genetically Engineered Mouse Model of Gastrointestinal Stromal Tumor
Published on: May 2, 2022
Imatinib inhibits oral squamous cell carcinoma by suppressing the PI3K/AKT/mTOR signaling pathway
Lei Ma1, Ke Huang1, Haibo Zhang2
1Department of Animal Science and Biotechnology, Research Center for Horse Industry, Kyungpook National University, Sangju, Gyeongsangbuk-do 37224, Republic of Korea.
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.
Insights
Imatinib effectively inhibits oral squamous cell carcinoma (OSCC) proliferation and viability. This study reveals imatinib
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Oral squamous cell carcinoma (OSCC) is a significant oral cancer with high mortality due to invasion and metastasis.
- Imatinib shows promise in treating various cancers, but its specific effects on OSCC require further investigation.
Purpose of the Study:
- To investigate the anticancer effects of imatinib on OSCC cells.
- To elucidate the underlying mechanisms of imatinib's action in OSCC.
Main Methods:
- Cell Counting Kit-8 assay for cell viability.
- Morphological analysis for proliferation.
- Wound-healing and soft agar assays for migration and colony formation.
- Flow cytometry for apoptosis analysis.
- Western blot to confirm molecular mechanisms.
Main Results:
- Imatinib significantly inhibited OSCC cell proliferation and viability in a dose- and time-dependent manner.
- Imatinib suppressed OSCC cell migration and colony formation.
- Imatinib induced apoptosis by modulating p53, Bax, PARP, and Bcl-2 expression.
- Imatinib inhibited the PI3K/AKT/mTOR signaling pathway.
Conclusions:
- Imatinib demonstrates potent anticancer effects against OSCC cells.
- Imatinib induces apoptosis and inhibits proliferation, migration, and colony formation in OSCC.
- Imatinib holds potential as a therapeutic agent for oral cancer treatment.
More Related Videos
Related Concept Videos
Inhibition of Cdk Activity
PI3K/mTOR/AKT Signaling Pathway
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Targeted Cancer Therapies
There are several types of targeted therapies against...
Mitogens and the Cell Cycle
Drugs that Stabilize Microtubules

