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长链非编码RNA通过靶向上调促进肾透明细胞癌进展。

LncRNA Promotes Clear Cell Renal Cell Carcinoma Progression by Targeting to Upregulate .

作者信息

Yang Yu, Gong Pengfeng, Yao Dongwei, Xue Dong, He Xiaozhou

机构信息

Department of Hepatopancreatobiliary Surgery, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, People's Republic of China.

Department of Urology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, People's Republic of China.

出版信息

Cancer Manag Res. 2021 Mar 11;13:2287-2294. doi: 10.2147/CMAR.S298649. eCollection 2021.

Abstract

BACKGROUND

Long noncoding RNAs (lncRNAs) have been regarded as crucial regulators in many cancers, including clear cell renal cell carcinoma (ccRCC). This research aimed to explore the biological role and molecular mechanism of lncRNA in ccRCC.

MATERIALS AND METHODS

The expression levels of and were examined by RT-qPCR. Cell viability, migration and invasion were examined by CCK-8 and transwell assays. Luciferase reporter and RIP assays were adopted to verify the interaction between and or .

RESULTS

It was found that expression was highly expressed in ccRCC tissues and cells, and patients with high expression of had a short overall survival time. Moreover, depletion attenuated ccRCC cell viability, migration and invasion. In addition, was confirmed as a downstream target of and was inversely regulated by , and was a target of . Functional assays demonstrated that silencing or addition abolished the inhibitory effects of knockdown on ccRCC progression.

CONCLUSION

The results of the present study indicated that accelerated the development and progression of ccRCC by upregulating via sponging , suggesting a potential therapeutic target for patients with ccRCC.

摘要

背景

长链非编码RNA(lncRNAs)被认为是包括透明细胞肾细胞癌(ccRCC)在内的多种癌症的关键调节因子。本研究旨在探讨lncRNA在ccRCC中的生物学作用和分子机制。

材料与方法

通过RT-qPCR检测[具体lncRNA名称1]和[具体lncRNA名称2]的表达水平。采用CCK-8和Transwell实验检测细胞活力、迁移和侵袭能力。采用荧光素酶报告基因和RIP实验验证[具体lncRNA名称1]与[具体lncRNA名称2]或[具体基因名称]之间的相互作用。

结果

发现[具体lncRNA名称1]在ccRCC组织和细胞中高表达,且[具体lncRNA名称1]高表达的患者总生存时间较短。此外,[具体lncRNA名称1]的缺失减弱了ccRCC细胞的活力、迁移和侵袭能力。另外,[具体lncRNA名称2]被证实为[具体lncRNA名称1]的下游靶点,并受到[具体lncRNA名称1]的反向调节,且[具体基因名称]是[具体lncRNA名称2]的靶点。功能实验表明,[具体lncRNA名称2]的沉默或[具体基因名称]的添加消除了[具体lncRNA名称1]敲低对ccRCC进展的抑制作用。

结论

本研究结果表明,[具体lncRNA名称1]通过海绵吸附[具体lncRNA名称2]上调[具体基因名称],从而加速ccRCC的发生发展,提示其可能是ccRCC患者的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b56/7959199/09f308c58ae9/CMAR-13-2287-g0001.jpg

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