LINC01572 通过调节 miRNA-338-5p/TTK 轴介导的 p53 来促进肺腺癌的恶性进展。

IF 2.8 4区 医学 Q2 PHARMACOLOGY & PHARMACY
Shilan Liu, Xiao Liu, Qinghui Yang, Chunhua Zeng, Gang Hu, Bochen Ren
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引用次数: 0

摘要

目的:肺癌是严重威胁人类健康的恶性肿瘤之一:肺癌是严重威胁人类健康的恶性肿瘤之一。长非编码 RNA(lncRNA)是影响肿瘤发生和发展的重要因素。然而,lncRNA在肺癌进展中的作用机制仍有待进一步探讨:本研究分析了 TCGA 数据库,发现 LINC01572 在肺腺癌(LUAD)组织中增高。随后,借助lncBase、TargetScan和mirDIP等数据库以及京都基因组百科全书(KEGG)富集分析,挖掘出LINC01572/miRNA-338-5p/TTK调控轴和下游p53信号通路。LINC01572在LUAD细胞中的作用通过CCK-8测定、流式细胞术、集落形成、Transwell和划痕愈合试验得到了验证。然后通过双荧光素酶和 RIP 分析验证了 LINC01572/TTK 与 miRNA-338-5p 的结合能力:研究结果表明,与正常细胞相比,LINC01572在LUAD细胞中的表达量升高。LINC01572的过表达促进了LUAD细胞的增殖和迁移特性,但抑制了细胞凋亡。抑制 LINC01572 则会导致相反的结果。此外,拯救实验显示,LINC01572 作为 miRNA-338-5p 的分子海绵,以 TTK 为靶点操纵 p53,从而促进 LUAD 细胞的恶性发展。此外,我们还构建了小鼠异种移植模型,并证实敲除 LINC01572 会阻碍 LUAD 实体瘤在体内的生长:我们的研究结果阐明了LINC01572影响LUAD的分子机制,为LUAD细胞的靶向治疗提供了新的思路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
LINC01572 promotes the malignant progression of lung adenocarcinoma by modulating p53 mediated by miRNA-338-5p/TTK axis.

Objectives: Lung cancer is one of the malignant tumors that threaten human health seriously. Long non-coding RNA (lncRNA) is an important factor affecting tumorigenesis and development. However, the mechanism of lncRNA in lung cancer progression remains to be further explored.

Methods: In this study, the TCGA database was analyzed, and LINC01572 was found to be increased in lung adenocarcinoma (LUAD) tissues. Thereafter, with the help of databases including lncBase, TargetScan, and mirDIP, as well as Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, LINC01572/miRNA-338-5p/TTK regulatory axis and downstream p53 signaling pathway were excavated. qRT-PCR was adopted to detect levels of LINC01572, miRNA-338-5p, and TTK in LUAD cells. The role that LINC01572 played in LUAD cells was validated by CCK-8 assay, flow cytometry, colony formation, Transwell, and scratch healing assays. The binding ability between LINC01572/TTK and miRNA-338-5p was then verified by dual-luciferase and RIP analysis.

Key findings: The results of this study demonstrated that LINC01572 was elevated in LUAD cells compared with normal cells. The overexpression of LINC01572 promoted the proliferative and migratory properties of LUAD cells but inhibited cell apoptosis. The inhibition of LINC01572 resulted in the opposite result. In addition, rescue experiments revealed that LINC01572, as a molecular sponge of miRNA-338-5p, targeted TTK to manipulate p53 for facilitating LUAD cell malignant progression. Apart from this, we constructed a mouse xenograft model and confirmed that the knockdown of LINC01572 hindered the growth of LUAD solid tumors in vivo.

Conclusions: Our findings illuminated the molecular mechanism of LINC01572 influencing LUAD and provided new insights for targeted therapy of LUAD cells.

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来源期刊
CiteScore
6.60
自引率
0.00%
发文量
91
审稿时长
3 months
期刊介绍: JPP keeps pace with new research on how drug action may be optimized by new technologies, and attention is given to understanding and improving drug interactions in the body. At the same time, the journal maintains its established and well-respected core strengths in areas such as pharmaceutics and drug delivery, experimental and clinical pharmacology, biopharmaceutics and drug disposition, and drugs from natural sources. JPP publishes at least one special issue on a topical theme each year.
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