In silico analysis of DYNLL1 expression in ovarian cancer chemoresistance.

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.