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Updated: Jul 26, 2025
Intramucosal Inoculation of Squamous Cell Carcinoma Cells in Mice for Tumor Immune Profiling and Treatment Response Assessment
Published on: April 22, 2019
Targeting eIF5A2 reduces invasion and reverses chemoresistance in SCC-9 cells in vitro
1Department of Stomatology, Tianjin Third Central Hospital, Hedong District, Tianjin, PR China. cityshanghai664@126.com.
Background And Aims:
Eukaryotic translation initiation factor 5A2 (EIF5A2) has been reported to be involved in metastasis and chemotherapy resistance in many human cancers. However, the effect and mechanism of EIF5A2 in oral cancer cells are unknown. Here, we investigated the effects of targeting EIF5A2 on chemotherapy resistance in oral cancer cells in vitro.
Methods:
By using a lentiviral system, we investigated the effects of targeting EIF5A2 on the invasion, migration, growth, and chemosensitivity of SCC-9 cells to CDDP in vitro. Through the method of gene intervention, we explore the role of pro-apoptotic Bim and epithelial and mesenchymal marker E-cadherin protein in this process and the regulation of EIF5A2 on Bim and E-cadherin.
Results:
Targeting EIF5A2 reduces invasion and migration in SCC-9 cells partly through upregulation of E-cadherin expression; Targeting EIF5A2 promotes cell apoptosis and inhibits cell survival as well as increasing chemosensitivity in SCC-9 cells through upregulation of Bim expression.
Conclusion:
EIF5A2 may be a novel potential therapeutic target for oral cancer by upregulation of Bim and E-cadherin.
Insights
Targeting eukaryotic translation initiation factor 5A2 (EIF5A2) in oral cancer cells reduces metastasis and enhances chemotherapy sensitivity. This is achieved by increasing Bim and E-cadherin expression, suggesting EIF5A2 as a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Eukaryotic translation initiation factor 5A2 (EIF5A2) is implicated in metastasis and chemotherapy resistance in various cancers.
- The role of EIF5A2 in oral cancer remains largely uncharacterized.
Purpose of the Study:
- To investigate the effects of targeting EIF5A2 on chemotherapy resistance in oral cancer cells.
- To elucidate the underlying mechanisms involving Bim and E-cadherin.
Main Methods:
- Utilized a lentiviral system to target EIF5A2 in SCC-9 oral cancer cells.
- Assessed the impact on cell invasion, migration, growth, and chemosensitivity to CDDP.
- Examined the expression levels of Bim and E-cadherin.
Main Results:
- Targeting EIF5A2 significantly reduced invasion and migration, associated with increased E-cadherin expression.
- EIF5A2 inhibition promoted apoptosis and enhanced chemosensitivity by upregulating Bim expression.
- These findings suggest EIF5A2 regulates key proteins involved in oral cancer progression and treatment response.
Conclusions:
- EIF5A2 inhibition presents a promising therapeutic strategy for oral cancer.
- Upregulation of Bim and E-cadherin mediates the anti-cancer effects of targeting EIF5A2.
- EIF5A2 is identified as a novel potential therapeutic target for oral cancer treatment.
