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CircRNA_101505 sensitizes hepatocellular carcinoma cells to cisplatin by sponging miR-103 and promotes oxidored-nitro domain-containing protein 1 expression
Cell Death Discovery ( IF 7 ) Pub Date : 2019-07-29 , DOI: 10.1038/s41420-019-0202-6
Yanwei Luo , Yunfeng Fu , Rong Huang , Meng Gao , Fengxia Liu , Rong Gui , Xinmin Nie

Hepatocellular carcinoma (HCC) is one of the most common malignant tumors and a leading cause of cancer-related deaths worldwide. Emerging studies have shown that circular RNAs (circRNAs) are differentially expressed in HCC and play an important role in HCC pathogenesis and metastasis. However, the mechanism of circRNA in the chemoresistance of HCC remains unclear. In this study, we aimed to investigate the role of circRNA in cisplatin resistance of HCC. We identified a novel circRNA circRNA_101505 that was decreased in cisplatin-resistant HCC tissues and cell lines, and associated with a poor survival outcome. Gain-of-function investigations showed that overexpression of circRNA_101505 suppressed cancer cell growth in vivo and in vitro, and enhanced cisplatin toxicity in HCC cells. Mechanistic studies found that circRNA_101505 could sensitize HCC cells to cisplatin by sponging miR-103, and thereby promoting oxidored-nitro domain-containing protein 1 (NOR1) expression. In conclusion, the significant inhibitory effects indicate circRNA_101505 to be a potential therapeutic target for HCC treatment. Our findings provide significant evidence to further elucidate the therapeutic use of circRNA in HCC.



中文翻译:

CircRNA_101505通过使miR-103变海绵使肝癌细胞对顺铂敏感,并促进含氧化氮结构域的蛋白1表达

肝细胞癌(HCC)是最常见的恶性肿瘤之一,并且是全球范围内与癌症相关的死亡的主要原因。新兴研究表明,环状RNA(circRNA)在HCC中差异表达,并在HCC发病机理和转移中起重要作用。然而,circRNA在肝癌化学耐药中的机制尚不清楚。在这项研究中,我们旨在研究circRNA在HCC的顺铂耐药性中的作用。我们鉴定了一种新的circRNA circRNA_101505,其在顺铂耐药的HCC组织和细胞系中降低,并且与不良的生存结果相关。功能获得的研究表明,circRNA_101505的过表达抑制了体内和体外癌细胞的生长,并增强了HCC细胞中顺铂的毒性。机理研究发现,circRNA_101505可以通过使miR-103海绵化,从而使HCC细胞对顺铂敏感,从而促进含氧化硝基域的蛋白1(NOR1)的表达。总之,显着的抑制作用表明circRNA_101505是HCC治疗的潜在治疗靶标。我们的发现为进一步阐明circRNA在HCC中的治疗用途提供了重要的证据。

更新日期:2019-11-18
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