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In silico analysis of DYNLL1 expression in ovarian cancer chemoresistance.
Cell Biology International ( IF 3.9 ) Pub Date : 2020-03-24 , DOI: 10.1002/cbin.11352
Caglar Berkel 1 , Ercan Cacan 1
Affiliation  

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.

中文翻译:

卵巢癌化学耐药性中DYNLL1表达的计算机分析。

卵巢癌(OC)是最致命的妇科癌症,化学耐药性是该疾病治疗失败和不良临床后果的原因。据报道,DYNLL1的缺失导致BRCA1突变的高级浆液性卵巢癌细胞的化学耐药性增加。考虑到其在化学抗性中的作用,需要对DYNLL1表达有更好的了解,以开发治疗OC的新策略。在当前的研究中,我们旨在研究DYNLL1在OC中相对于细胞类型,化学敏感性概况,某些药物治疗和癌症进展的差异表达。DYNLL1使用来自Gene Expression Omnibus的表达谱数据集和R中的定量逆转录聚合酶链反应分析血红蛋白的水平。我们发现,与正常卵巢细胞相比,OC组织型中DYNLL1的水平更高。DYNLL1表达在上皮型OC细胞中降低;但是,与匹配的对照细胞相比,它在基质型OC细胞中增加。化学抗性OC细胞显示出比化学敏感性OC细胞更低的DYNLL1表达。卡铂和NSC319726处理导致DYNLL1DYNLL1表达略有下降OC上皮细胞在癌症进展过程中血脂水平降低。结果表明,OC中DYNLL1表达的变化可能与细胞类型有关,而较低的DYNLL1水平可能与OC中的化学抗性增加有关。尽管需要进一步的研究,但某些药物和癌症的进展可能导致DYNLL1水平降低,可能导致化学耐药性增加。因此,可以说DYNLL1可能是OC进展和化学抗性的重要参与者。
更新日期:2020-03-24
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