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Long Noncoding RNA KIF9-AS1 Regulates Transforming Growth Factor-β and Autophagy Signaling to Enhance Renal Cell Carcinoma Chemoresistance via microRNA-497-5p.
DNA and Cell Biology ( IF 3.1 ) Pub Date : 2020-07-02 , DOI: 10.1089/dna.2020.5453
Yichen Jin 1 , Ru Huang 1 , Yanfu Xia 1 , Chen Huang 1 , Feng Qiu 1 , Jinxian Pu 1 , Xuefeng He 1 , Xiaojun Zhao 1
Affiliation  

Renal cell carcinoma (RCC) has been regarded as one of the most malignant tumor types. Chemotherapy (such as sorafenib) is used as common strategy for treating RCC. To date, whether long noncoding RNA KIF9-AS1 is involved in RCC progression and drug resistance remains unknown. In this investigation, we detected gene expression levels by western blot and RT-qPCR. MTT and TUNEL experiments were used to show cell viability and apoptosis, respectively. KIF9-AS1 overexpression led to enhanced cell viability, increased IC50 value of sorafenib, and decreased apoptosis. miR-497-5p acted as key interaction factor for KIF9-AS1 in RCC. More importantly, we found that transforming growth factor-β and autophagy signaling pathways were both critical effectors for mediating KIF9-AS1/miR-497-5p axis-induced drug resistance phenotypes (cell viability, IC50, apoptosis) of RCC. In conclusion, our study revealed that KIF9-AS1 played a positive role in drug resistance of RCC cells to sorafenib, potentially driving the development of targeted diagnostic and therapeutical approaches.

中文翻译:

长非编码RNA KIF9-AS1通过microRNA-497-5p调节转化生长因子-β和自噬信号,增强肾细胞癌的化学耐药性。

肾细胞癌(RCC)被认为是最恶性的肿瘤类型之一。化学疗法(例如索拉非尼)被用作治疗RCC的常见策略。迄今为止,RCC进展和耐药性是否涉及长的非编码RNA KIF9-AS1仍是未知的。在这项研究中,我们通过蛋白质印迹和RT-qPCR检测基因表达水平。使用MTT和TUNEL实验分别显示细胞活力和凋亡。KIF9-AS1过表达导致细胞活力增强,IC 50升高价值索拉非尼,并减少凋亡。miR-497-5p是RCC中KIF9-AS1的关键相互作用因子。更重要的是,我们发现转化生长因子-β和自噬信号通路均是介导KIF9-AS1 / miR-497-5p轴诱导的RCC耐药性表型(细胞生存力,IC 50和细胞凋亡)的关键效应器。总之,我们的研究表明,KIF9-AS1在RCC细胞对索拉非尼的耐药性中发挥了积极作用,可能推动了靶向诊断和治疗方法的发展。
更新日期:2020-07-10
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