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Bioinformatics approach combined with experimental verification reveals OAS3 gene implicated in paclitaxel resistance
Hasan Onur Caglar1, Abdulmelik Aytatli1,2, Neslisah Barlak1,2
1Department of Molecular Biology and Genetics, Faculty of Science, Erzurum Technical University, Erzurum, Turkey.
Background:
This study aimed to identify a candidate gene associated with paclitaxel (PTX) resistance and to evaluate functionally its biological role in the PTX-resistant head and neck squamous cell carcinoma (HNSCC) cell lines and clinical specimens.
Methods:
Microarray data series containing samples of different types of cancers resistant to PTX were analyzed and then a candidate gene associated with PTX resistance was identified using various bioinformatics tools. After the suppression of the target gene expression, changes in cell viability and colony-forming ability were evaluated in PTX-resistant FaDu and SCC-9 cell lines.
Results:
Bioinformatics analyses of upregulated genes in PTX-resistant cancer cells indicated that OAS3 was associated with PTX resistance. The downregulation of OAS3 expression significantly reduced the viability and colony-forming capacity of PTX-resistant SCC-9 cells by inducing apoptosis and cell cycle arrest at G0/G1 phase.
Conclusions:
The therapeutic targeting of OAS3 may resensitize PTX-resistant HNSCC cells with high OAS3 expression to PTX treatment.
Insights
Researchers identified OAS3 as a key gene in paclitaxel (PTX) resistance in head and neck squamous cell carcinoma (HNSCC). Targeting OAS3 may restore PTX sensitivity in resistant HNSCC tumors.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Paclitaxel (PTX) resistance is a significant challenge in treating head and neck squamous cell carcinoma (HNSCC).
- Identifying novel therapeutic targets is crucial for overcoming PTX resistance in HNSCC.
Purpose of the Study:
- To identify a candidate gene linked to PTX resistance in HNSCC.
- To functionally characterize the biological role of the candidate gene in PTX-resistant HNSCC.
Main Methods:
- Analysis of microarray data from PTX-resistant cancer samples using bioinformatics tools.
- Gene expression suppression in PTX-resistant HNSCC cell lines (FaDu and SCC-9).
- Evaluation of cell viability, colony formation, apoptosis, and cell cycle progression.
Main Results:
- Bioinformatics analysis identified OAS3 as significantly upregulated in PTX-resistant cancers.
- Downregulation of OAS3 in SCC-9 cells reduced cell viability and colony formation.
- OAS3 suppression induced apoptosis and G0/G1 cell cycle arrest in PTX-resistant cells.
Conclusions:
- OAS3 is a potential therapeutic target for overcoming PTX resistance in HNSCC.
- Targeting OAS3 may resensitize PTX-resistant HNSCC cells to paclitaxel treatment.
