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FTX通过靶向miR-335-5p/NUCB2轴促进肺腺癌中的细胞增殖和迁移。

FTX contributes to cell proliferation and migration in lung adenocarcinoma via targeting miR-335-5p/NUCB2 axis.

作者信息

Huo Xiaodong, Wang Huixing, Huo Bin, Wang Lei, Yang Kuo, Wang Jinhuan, Wang Lili, Wang Haitao

机构信息

1Department of Oncology, The Second Hospital of Tianjin Medical University, No. 23 Pingjiang Road, Hexi District, Tianjin, 300211 China.

2Pain Management Center, The Second Hospital of Tianjin Medical University, Tianjin, 300211 China.

出版信息

Cancer Cell Int. 2020 Mar 23;20:89. doi: 10.1186/s12935-020-1130-5. eCollection 2020.

DOI:10.1186/s12935-020-1130-5
PMID:32226311
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7092578/
Abstract

BACKGROUND

Extensive studies revealed that long non-coding RNAs (lncRNAs) could act as a regulator in tumors, including lung adenocarcinoma (LUAD). LncRNA FTX transcript, XIST regulator (FTX) has been reported to regulate the biological behaviors of some cancers. Nevertheless, its functional role and molecular mechanism remain obscure in LUAD. Our current study concentrates on exploring the biological function of FTX in LUAD.

METHODS

RT-qPCR was used to test the expression of FTX, miR-335-5p or NUCB2 in LUAD cells. The effect of FTX on LUAD progression was investigated by colony formation, EdU, flow cytometry, TUNEL, transwell and western blot assays. The interaction between microRNA-335-5p (miR-335-5p) and FTX or nucleobindin 2 (NUCB2) was confirmed by luciferase reporter assay.

RESULTS

RT-qPCR showed that FTX expression was up-regulated in LUAD cell lines. Loss-of-function assay indicated that FTX accelerated cell proliferation, migration and invasion, while inhibited cell apoptosis in LUAD. Besides, miR-335-5p, lowly expressed in LUAD cells, was discovered to be sponged by FTX. Subsequently, NUCB2 was identified as a target gene of miR-335-5p. Additionally, it was confirmed that NUCB2 functioned as an oncogene in LUAD. Rescue assays indicated that LUAD progression inhibited by FTX knockdown could be restored by NUCB2 up-regulation.

CONCLUSION

FTX played an oncogenic role in LUAD and contributed to cancer development via targeting miR-335-5p/NUCB2 axis.

摘要

背景

大量研究表明，长链非编码RNA（lncRNA）可作为肿瘤（包括肺腺癌，LUAD）的调节因子。据报道，lncRNA FTX转录本，XIST调节因子（FTX）可调节某些癌症的生物学行为。然而，其在LUAD中的功能作用和分子机制仍不清楚。我们目前的研究集中于探索FTX在LUAD中的生物学功能。

方法

采用RT-qPCR检测LUAD细胞中FTX、miR-335-5p或NUCB2的表达。通过集落形成、EdU、流式细胞术、TUNEL、Transwell和蛋白质印迹分析研究FTX对LUAD进展的影响。通过荧光素酶报告基因检测证实微小RNA-335-5p（miR-335-5p）与FTX或核结合蛋白2（NUCB2）之间的相互作用。

结果

RT-qPCR显示FTX在LUAD细胞系中表达上调。功能丧失分析表明，FTX促进LUAD细胞增殖、迁移和侵袭，同时抑制细胞凋亡。此外，发现LUAD细胞中低表达的miR-335-5p被FTX吸附。随后，NUCB2被鉴定为miR-335-5p的靶基因。此外，证实NUCB2在LUAD中起癌基因作用。挽救分析表明，上调NUCB2可恢复因敲低FTX而抑制的LUAD进展。

结论

FTX在LUAD中发挥致癌作用，并通过靶向miR-335-5p/NUCB2轴促进癌症发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc5/7092578/2470b5b21f56/12935_2020_1130_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc5/7092578/0fe391a33898/12935_2020_1130_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc5/7092578/b988aa3a0eee/12935_2020_1130_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc5/7092578/0414e7fc53b0/12935_2020_1130_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc5/7092578/82834a653047/12935_2020_1130_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc5/7092578/2470b5b21f56/12935_2020_1130_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc5/7092578/0fe391a33898/12935_2020_1130_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc5/7092578/b988aa3a0eee/12935_2020_1130_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc5/7092578/0414e7fc53b0/12935_2020_1130_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc5/7092578/82834a653047/12935_2020_1130_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc5/7092578/2470b5b21f56/12935_2020_1130_Fig5_HTML.jpg

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