LncRNA FOXP4-AS promotes the progression of non-small cell lung cancer by regulating the miR-3184-5p/EIF5A axis

IF 3.1 3区 生物学 Q2 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Journal of Tissue Engineering and Regenerative Medicine Pub Date : 2021-12-18 DOI:10.1002/term.3275
Dingbiao Li, Zhenhua Li, Wang YanFei, Ying Wang, Jianlin Shi, Chang Liu, Laihao Qu, Shoujun Deng, Dalin Xiong
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引用次数: 3

Abstract

Long non coding RNA FOXP4-AS1 exerted crucial functions in various human cancers, while its role in non-small cell lung cancer (NSCLC) remains unclear. A total of 30 pairs of NSCLC tissues and matched adjacent normal tissues were used to evaluate the expression of FOXP4-AS1 and miR-3184-5p. Cell proliferation was assessed by CCK-8 assay and colony formation assay. Cell apoptosis was measured by flow cytometry. Bioinformatic analysis and luciferase reporter assay were performed to determine the regulatory relationship among FOXP4-AS1, miR-3184-5p and EIF5A. The xenograft tumor model was constructed to confirm the function of FOXP4-AS1 in NSCLC progression. The results showed that FOXP4-AS1 was upregulated and miR-3184-5p was downregulated in NSCLC tissues and cell lines. Downregulation of FOXP4-AS1 significantly reduced cell proliferation and induced apoptosis of NSCLC cells in vitro. FOXP4-AS1 could regulated the expression of EIF5A by binding to miR-3184-5p. Rescue experiments showed that downregulation of miR-3184-5p or overexpression of EIF5A obviously attenuated the inhibitory effects of si-FOXP4-AS1 on cell proliferation, as well as the stimulating effects on cell apoptosis. Moreover, knockdown of FOXP4-AS1 could efficiently inhibited tumor development of NSCLC in vivo. Downregulation of FOXP4-AS1 attenuated the progression of NSCLC by regulating miR-3184-5p and EIF5A.

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LncRNA FOXP4-AS通过调控miR-3184-5p/EIF5A轴促进非小细胞肺癌的进展
长链非编码RNA FOXP4-AS1在多种人类癌症中发挥重要作用,但其在非小细胞肺癌(NSCLC)中的作用尚不清楚。采用30对NSCLC组织和匹配的邻近正常组织评估FOXP4-AS1和miR-3184-5p的表达。CCK-8法和菌落形成法检测细胞增殖情况。流式细胞术检测细胞凋亡。通过生物信息学分析和荧光素酶报告基因检测来确定FOXP4-AS1、miR-3184-5p和EIF5A之间的调控关系。构建异种移植肿瘤模型,证实FOXP4-AS1在NSCLC进展中的作用。结果显示,在NSCLC组织和细胞系中,FOXP4-AS1表达上调,miR-3184-5p表达下调。下调FOXP4-AS1可显著降低体外NSCLC细胞的增殖并诱导细胞凋亡。FOXP4-AS1可通过结合miR-3184-5p调控EIF5A的表达。救援实验表明,下调miR-3184-5p或过表达EIF5A可明显减弱si-FOXP4-AS1对细胞增殖的抑制作用和对细胞凋亡的刺激作用。此外,FOXP4-AS1基因敲低可以有效抑制NSCLC体内肿瘤的发展。FOXP4-AS1的下调通过调节miR-3184-5p和EIF5A来减缓NSCLC的进展。
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来源期刊
CiteScore
7.50
自引率
3.00%
发文量
97
审稿时长
4-8 weeks
期刊介绍: Journal of Tissue Engineering and Regenerative Medicine publishes rapidly and rigorously peer-reviewed research papers, reviews, clinical case reports, perspectives, and short communications on topics relevant to the development of therapeutic approaches which combine stem or progenitor cells, biomaterials and scaffolds, growth factors and other bioactive agents, and their respective constructs. All papers should deal with research that has a direct or potential impact on the development of novel clinical approaches for the regeneration or repair of tissues and organs. The journal is multidisciplinary, covering the combination of the principles of life sciences and engineering in efforts to advance medicine and clinical strategies. The journal focuses on the use of cells, materials, and biochemical/mechanical factors in the development of biological functional substitutes that restore, maintain, or improve tissue or organ function. The journal publishes research on any tissue or organ and covers all key aspects of the field, including the development of new biomaterials and processing of scaffolds; the use of different types of cells (mainly stem and progenitor cells) and their culture in specific bioreactors; studies in relevant animal models; and clinical trials in human patients performed under strict regulatory and ethical frameworks. Manuscripts describing the use of advanced methods for the characterization of engineered tissues are also of special interest to the journal readership.
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