长非编码 RNA PTPRG 反义 RNA 1 靶向 Cyclin D1 促进肺腺癌细胞增殖

IF 2.4 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
Cancer Biotherapy and Radiopharmaceuticals Pub Date : 2024-10-01 Epub Date: 2021-11-12 DOI:10.1089/cbr.2021.0168
Yang Xue, Mingqiang Diao, Jing Lyu, Kang Li, Long He, Junfeng Chen, Xiangguo Li
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引用次数: 0

摘要

背景:许多研究记录了长非编码RNA(lncRNA)在癌症发展中的功能,包括肺腺癌(LUAD)。之前的研究报道了 lncRNA PTPRG antisense RNA 1(PTPRG-AS1)在各种癌症中的关键作用。然而,PTPRG-AS1在LUAD中的作用仍然未知。材料与方法:应用实时定量聚合酶链反应(RT-qPCR)检测 PTPRG-AS1 在 LUAD 细胞系中的表达。功能测试和体内实验探讨了细胞增殖,而流式细胞仪分析则用于检测细胞周期。此外,荧光原位杂交(FISH)和亚细胞分馏试验也检测了 PTPRG-AS1 在 LUAD 细胞中的定位。利用RNA pulldown、荧光素酶报告和RNA免疫沉淀(RIP)实验研究了PTPRG-AS1/miR-124-3p/细胞周期蛋白D1(CCND1)轴的相互作用。结果PTPRG-AS1在LUAD细胞系中明显高表达。PTPRG-AS1 基因敲除抑制了细胞的增殖和周期以及 CCND1 的水平。此外,miR-124-3p 是 PTPRG-AS1 和 CCND1 的共同靶标。此外,PTPRG-AS1还能上调LUAD细胞中的CCND1。此外,miR-124-3p 的消耗逆转了 PTPRG-AS1 沉默对 LUAD 细胞行为的抑制作用,但随后 CCND1 的敲除抵消了下调的 miR-124-3p 的促进作用。结论PTPRG-AS1通过靶向miR-124-3p/CCND1轴促进了LUAD的细胞增殖和细胞周期。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Long Noncoding RNAs PTPRG Antisense RNA 1 Targets Cyclin D1 to Facilitate Cell Proliferation in Lung Adenocarcinoma.

Background: Numerous studies have recorded the function of long noncoding RNAs (lncRNAs) in cancer development, including lung adenocarcinoma (LUAD). Previous studies have reported the crucial role of lncRNA PTPRG antisense RNA 1 (PTPRG-AS1) in various cancers. However, the role of PTPRG-AS1 in LUAD remains unknown. Materials and Methods: Real-time quantitative polymerase chain reaction (RT-qPCR) was applied for detecting PTPRG-AS1 expression in LUAD cell lines. Functional assays and in vivo experiments explored cell proliferation, whereas flow cytometry analysis was used to detect cell cycle. In addition, fluorescent in situ hybridization (FISH) and subcellular fractionation assay measured the localization of PTPRG-AS1 in LUAD cells. RNA pulldown, luciferase reporter, and RNA immunoprecipitation (RIP) assays were used to investigate the interaction of PTPRG-AS1/miR-124-3p/cyclin D1 (CCND1) axis. Results: PTPRG-AS1 expression was notably high in LUAD cell lines. PTPRG-AS1 knockdown suppressed cell proliferation and cycle as well as the level of CCND1. Moreover, miR-124-3p was the mutual target of PTPRG-AS1 and CCND1. In addition, PTPRG-AS1 sponged miR-124-3p to upregulate CCND1 in LUAD cells. Moreover, miR-124-3p depletion reversed the suppression of PTPRG-AS1 silence on LUAD cell behaviors, but then CCND1 knockdown countervailed the promoting influence of downregulated miR-124-3p. Conclusions: PTPRG-AS1 propels cell proliferation and cell cycle of LUAD by targeting miR-124-3p/CCND1 axis.

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来源期刊
CiteScore
7.80
自引率
2.90%
发文量
87
审稿时长
3 months
期刊介绍: Cancer Biotherapy and Radiopharmaceuticals is the established peer-reviewed journal, with over 25 years of cutting-edge content on innovative therapeutic investigations to ultimately improve cancer management. It is the only journal with the specific focus of cancer biotherapy and is inclusive of monoclonal antibodies, cytokine therapy, cancer gene therapy, cell-based therapies, and other forms of immunotherapies. The Journal includes extensive reporting on advancements in radioimmunotherapy, and the use of radiopharmaceuticals and radiolabeled peptides for the development of new cancer treatments.
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