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长链非编码RNA MALAT1通过靶向骨肉瘤中的miR-590-3p促进细胞增殖、迁移和侵袭。

Long non-coding RNA MALAT1 promotes cell proliferation, migration and invasion by targeting miR-590-3p in osteosarcoma.

作者信息

Zhao Hui, Wang Yongping, Hou Weihua, Ding Xuanxi, Wang Wenji

机构信息

Department of Orthopedics, First Hospital of Lanzhou University, Lanzhou, Gansu 730000, P.R. China.

出版信息

Exp Ther Med. 2022 Sep 14;24(5):672. doi: 10.3892/etm.2022.11608. eCollection 2022 Nov.

Abstract

Osteosarcoma (OS) is a common malignant bone cancer and commonly occurs in adolescents and children. Long non-coding RNAs (lncRNAs) play major roles in cancer cell proliferation and metastasis. The present study aimed to investigate the potential molecular mechanism of lncRNA MALAT1 in OS. The levels of lncRNA MALAT1 and microRNA-590-3p were detected by reverse transcription-quantitative PCR in OS tissues and cells. Cell Counting Kit-8 and flow cytometry assays were conducted to assess cell proliferation and apoptosis. Cell migration and invasion were examined by Transwell assay. The levels of E-cadherin, N-Cadherin, Vimentin and Snail were measured by western blotting. The target of MALAT1 was predicted using online software and confirmed by luciferase reporter, RNA immunoprecipitation and RNA pull-down assays. The results indicated that MALAT1 was highly expressed in OS tissues and cell lines. MALAT1 knockdown promoted apoptosis and suppressed proliferation, migration, invasion and epithelial- mesenchymal transition (EMT) of OS cells. Overexpression of miR-590-3p increased cell apoptosis and hampered cell proliferation, migration, invasion and EMT in OS cells. In addition, MALAT1 knockdown upregulated the expression of miR-590-3p in OS cells. In conclusion, MALAT1 was demonstrated to suppress cell apoptosis and induce cell proliferation, migration, invasion and EMT by inhibiting miR-590-3p in OS, which indicated that MALAT1 has potential value in the diagnosis and treatment of OS.

摘要

骨肉瘤(OS)是一种常见的恶性骨癌,常见于青少年和儿童。长链非编码RNA(lncRNA)在癌细胞增殖和转移中起主要作用。本研究旨在探讨lncRNA MALAT1在骨肉瘤中的潜在分子机制。采用逆转录定量PCR检测骨肉瘤组织和细胞中lncRNA MALAT1和微小RNA-590-3p的水平。进行细胞计数试剂盒-8和流式细胞术检测以评估细胞增殖和凋亡。通过Transwell检测法检测细胞迁移和侵袭。采用蛋白质免疫印迹法检测E-钙黏蛋白、N-钙黏蛋白、波形蛋白和Snail的水平。使用在线软件预测MALAT1的靶标,并通过荧光素酶报告基因、RNA免疫沉淀和RNA下拉试验进行验证。结果表明,MALAT1在骨肉瘤组织和细胞系中高表达。敲低MALAT1可促进骨肉瘤细胞凋亡,抑制其增殖、迁移、侵袭和上皮-间质转化(EMT)。过表达miR-590-3p可增加骨肉瘤细胞凋亡,并阻碍其增殖、迁移、侵袭和EMT。此外,敲低MALAT1可上调骨肉瘤细胞中miR-590-3p的表达。总之,研究表明MALAT1通过抑制miR-590-3p来抑制骨肉瘤细胞凋亡,并诱导其增殖、迁移、侵袭和EMT,这表明MALAT1在骨肉瘤的诊断和治疗中具有潜在价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5402/9533361/893ab14aa6b1/etm-24-05-11608-g00.jpg

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