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长链非编码 RNA 通过靶向 miR-148a-3p 调控 c-Met 促进宫颈癌进展。

Long non-coding RNA promotes cervical cancer progression through regulating c-Met via targeting miR-148a-3p.

机构信息

Foreign Department-Department of Clinical Medicine, Pavlov First Saint Petersburg State Medical University, St. Petersburg, Russian Federation.

出版信息

Cell Cycle. 2019 Dec;18(23):3313-3324. doi: 10.1080/15384101.2019.1674071. Epub 2019 Oct 7.

Abstract

Long non-coding RNA (lncRNA)  has been shown to be associated with the development of a variety of cancers. The purpose of this study was to investigate the effect of  on cervical cancer (CC) and the corresponding mechanism. The qRT-PCR was used to determine the expressions of SNHG4 and  in CC cell lines and tissues. Cell apoptosis and proliferation were measured by flow cytometry and MTT assay, respectively. The interaction between SNHG4,  and  was verified by bioinformatics, dual-luciferase reporter gene and RNA immunoprecipitation (RIP), and the effect of  on the growth of CC tumor  was explored. The expression of  was increased in both CC cell lines and tissues, while the expression of  was down-regulated. Meanwhile, silencing SNHG4 remarkably inhibited CC cell proliferation and promoted apoptosis. In addition, miR-148a-3p was a direct target gene of , and down-regulation of miR-148a-3p could observably reverse the effect of silencing  on the proliferation and apoptosis of CC cells. More importantly,  could up-regulate the expression of  by targeting and interacting with . Finally,  experiments confirmed that silence SNHG4 down-regulated the expression of  by promoting , and ultimately suppressed the growth of CC tumor . In conclusion,  could be used as a competitive endogenous RNA to bind to miR-148a-3p, thereby up-regulating the expression of  and ultimately promoting the progression of CC, which provided a potential therapeutic target for the targeted treatment of CC.

摘要

长链非编码 RNA(lncRNA)已被证明与多种癌症的发生有关。本研究旨在探讨 SNHG4 在宫颈癌(CC)中的作用及其相应机制。qRT-PCR 用于测定 CC 细胞系和组织中 SNHG4 和 的表达。通过流式细胞术和 MTT 测定分别测量细胞凋亡和增殖。通过生物信息学、双荧光素酶报告基因和 RNA 免疫沉淀(RIP)验证 SNHG4 和 的相互作用,并探讨 的表达对 CC 肿瘤生长的影响。结果表明,在 CC 细胞系和组织中均上调了 的表达,而 的表达下调。同时,沉默 SNHG4 显著抑制 CC 细胞增殖并促进凋亡。此外,miR-148a-3p 是 的直接靶基因,下调 miR-148a-3p 可明显逆转沉默 对 CC 细胞增殖和凋亡的影响。更重要的是, 通过靶向和相互作用可以上调 的表达。最后, 实验证实,沉默 SNHG4 通过促进 来下调 的表达,从而最终抑制 CC 肿瘤的生长。综上所述, 可以作为竞争性内源性 RNA 与 miR-148a-3p 结合,从而上调 的表达,最终促进 CC 的进展,为 CC 的靶向治疗提供了潜在的治疗靶点。

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