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长链非编码RNA B4GALT1-AS1通过海绵吸附miR-144-3p增加ZEB1水平,从而促进非小细胞肺癌细胞生长。

LncRNA B4GALT1-AS1 promotes non-small cell lung cancer cell growth via increasing ZEB1 level by sponging miR-144-3p.

作者信息

Liu Shi-Wei, Yang Pu, Li Fan-Nian, Dou Rui-Gang, Liu Jun-Xiao, Liu Guang-Jie

机构信息

Department of Thoracic surgery, The First Affiliated Hospital of Xingtai Medical College, Xingtai, China.

Department of Thoracic Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.

出版信息

Transl Cancer Res. 2022 Mar;11(3):538-547. doi: 10.21037/tcr-22-296.

Abstract

BACKGROUND

Long noncoding RNAs (lncRNAs) are emerging as key players in the development and progression of cancer. Several malignancies involve dysregulated long noncoding ribonucleic acids (lncRNAs) in non-small cell lung cancer cell growth and their aggressive phenotypes. LncRNA B4GALT1-AS1 is important in the advancement of various malignancies, although its contribution to non-small cell lung cancer (NSCLC) remains unexplored.

METHODS

LncRNA B4GALT1-AS1 in NSCLC tissues was detected and further validated in a cohort of non-small cell lung cancer tissues. The effects of lncRNA B4GALT1-AS1 on proliferation were determined by experiments. The B4GALT1-AS1-miR-144-3p-ZEB1 axis was assessed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Furthermore, the mechanism of B4GALT1-AS1 was investigated using loss-of-function assays .

RESULTS

We showed significant upregulation of B4GALT1-AS1 in cell lines and tissues of NSCLC. B4GALT1-AS1 knockdown impeded the proliferation-related characteristics of the NSCLC cells. The demonstration of the binding capacity of B4GALT1-AS1 and miR-144-3p was predicted by bioinformatics and luciferase reporter activity assay. The B4GALT1-AS1 and miR-144-3p interaction was shown by using rescue experiments. NSCLC has a positive association with its target, zinc finger e-box binding homeobox 1 (ZEB1).

CONCLUSIONS

In summary, the progression of NSCLC was facilitated by lncRNA B4GALT1-AS1 via interaction with miR-144-3p and positive regulation of ZEB1 expression.

摘要

背景

长链非编码RNA(lncRNAs)正成为癌症发生和发展的关键因素。几种恶性肿瘤在非小细胞肺癌细胞生长及其侵袭性表型中涉及长链非编码核糖核酸(lncRNAs)失调。lncRNA B4GALT1-AS1在多种恶性肿瘤进展中起重要作用,尽管其对非小细胞肺癌(NSCLC)的作用仍未被探索。

方法

检测NSCLC组织中的lncRNA B4GALT1-AS1,并在一组非小细胞肺癌组织中进一步验证。通过实验确定lncRNA B4GALT1-AS1对增殖的影响。通过双荧光素酶报告基因和RNA免疫沉淀(RIP)实验评估B4GALT1-AS1-miR-144-3p-ZEB1轴。此外,使用功能丧失实验研究B4GALT1-AS1的机制。

结果

我们发现NSCLC细胞系和组织中B4GALT1-AS1显著上调。敲低B4GALT1-AS1可阻碍NSCLC细胞的增殖相关特性。通过生物信息学和荧光素酶报告基因活性实验预测了B4GALT1-AS1与miR-144-3p的结合能力。通过拯救实验证明了B4GALT1-AS1与miR-144-3p的相互作用。NSCLC与其靶标锌指E盒结合同源框1(ZEB1)呈正相关。

结论

总之,lncRNA B4GALT1-AS1通过与miR-144-3p相互作用并正向调节ZEB1表达促进NSCLC进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a740/8990218/906807cbddaa/tcr-11-03-538-f1.jpg

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