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In silico analysis of DYNLL1 expression in ovarian cancer chemoresistance
1Department of Molecular Biology and Genetics, Tokat Gaziosmanpasa University, Tokat, Turkey.
Abstract:
Ovarian cancer (OC) is the most lethal gynecological cancer and chemoresistance is responsible for the treatment failure and unfavorable clinical outcome in this disease. The deletion of DYNLL1 was reported to result in increased chemoresistance in BRCA1-mutant high-grade serous ovarian carcinoma cells. Considering its role in chemoresistance, a better understanding of DYNLL1 expression is needed to develop novel strategies in the treatment of OC. In the current study, we aimed to investigate the differential expression of DYNLL1 in OC with respect to cell types, chemosensitivity profiles, certain drug treatments, and cancer progression. DYNLL1 levels were analyzed using expression profiling data sets from Gene Expression Omnibus and quantitative reverse-transcription polymerase chain reaction in R. We found that the level of DYNLL1 was higher in OC histotypes compared with normal ovarian cells. DYNLL1 expression is decreased in OC cells of epithelial type; but, it is increased in OC cells of stromal type, compared with matched control cells. Chemoresistant OC cells were shown to have lower DYNLL1 expression than chemosensitive OC cells. Carboplatin and NSC319726 treatments resulted in slightly decreased DYNLL1 expression and DYNLL1 levels were decreased in the course of cancer progression in OC epithelial cells. The results suggest that changes in DYNLL1 expression in OC might be cell-type dependent and lower DYNLL1 levels may be associated with increased chemoresistance in OC. Although further studies are needed, certain drugs and cancer progression may lead to lower DYNLL1 levels, possibly resulting in increased chemoresistance. Therefore, it can be stated that DYNLL1 might be an important player in OC progression and chemoresistance.
Insights
DYNLL1 expression varies in ovarian cancer (OC) cells, with lower levels linked to increased chemoresistance. Understanding these changes is key for developing new OC treatments.
Area of Science:
- Gynecologic Oncology
- Cancer Biology
- Molecular Oncology
Background:
- Ovarian cancer (OC) is a leading cause of cancer death, with treatment failure often due to chemoresistance.
- The protein DYNLL1 has been implicated in chemoresistance, particularly in BRCA1-mutant ovarian cancer.
- Further investigation into DYNLL1 expression is crucial for developing novel therapeutic strategies against OC.
Purpose of the Study:
- To investigate the differential expression of DYNLL1 in ovarian cancer.
- To correlate DYNLL1 levels with OC cell types, chemosensitivity, drug treatments, and cancer progression.
Main Methods:
- Analysis of Gene Expression Omnibus datasets.
- Quantitative reverse-transcription polymerase chain reaction (RT-qPCR) in R.
- Comparison of DYNLL1 levels across different OC histotypes, cell types, and treatment conditions.
Main Results:
- DYNLL1 levels were elevated in OC histotypes compared to normal ovarian cells.
- DYNLL1 expression decreased in epithelial OC cells but increased in stromal OC cells.
- Chemoresistant OC cells exhibited lower DYNLL1 expression than chemosensitive cells.
- Carboplatin and NSC319726 treatments slightly reduced DYNLL1 expression.
- DYNLL1 levels decreased during cancer progression in OC epithelial cells.
Conclusions:
- DYNLL1 expression in OC is cell-type dependent.
- Lower DYNLL1 levels are associated with increased chemoresistance in ovarian cancer.
- DYNLL1 may play a significant role in OC progression and chemoresistance, warranting further study.
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