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长链非编码RNA PCAT6通过调控miR-330-5p促进非小细胞肺癌细胞的增殖、迁移和侵袭。

lncRNA PCAT6 promotes non-small cell lung cancer cell proliferation, migration and invasion through regulating miR-330-5p.

作者信息

Cui Li Hua, Xu Hai Rong, Yang Wu, Yu Li Jiang

机构信息

Department of Oncology, People's Hospital of Jingjiang, Jingjiang, China,

Department of Oncology, The Northern Jiangsu People's Hospital, Yangzhou, China.

出版信息

Onco Targets Ther. 2018 Nov 1;11:7715-7724. doi: 10.2147/OTT.S178597. eCollection 2018.

DOI:10.2147/OTT.S178597
PMID:30464520
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6219114/
Abstract

BACKGROUND

Investigating the roles of lncRNA prostate cancer-associated transcript 6 (PCAT6) in modulating the growth and aggressiveness of non-small-cell lung carcinoma (NSCLC) cell.

METHOD

The levels of PCAT6 in NSCLC tissues and cell lines were determined by quantitative real-time PCR assay. MTT as well as colony formation assays were applied to explore the effect of PCAT6 on the growth of NSCLC cell in vitro. Wound healing and Transwell assays were utilized to analyze the impact of PCAT6 on the migration and invasion of NSCLC cell. Bioinformatics analysis and luciferase reporter assay were used to prove that miR-330-5p was the target of PCAT6. Colony formation, wound healing, and Transwell invasion assays were applied to demonstrate that PCAT6 promoted NSCLC cell growth, migration, and invasion through binding miR-330-5p. Finally, xenograft model was used to explore the role of PCAT6 in the tumor growth of NSCLC cell in vivo.

RESULTS

PCAT6 was highly overexpressed in NSCLC tissues and cells compared with normal tissues and non-tumorigenic bronchial epithelial cell line, BEAS-2B. Downregulation of PCAT6 markedly reduced the proliferation, migration, and invasion of NSCLC cell. Moreover, down-expression of PCAT6 significantly increased the level of miR-330-5p in NSCLC cell. Further functional experiments indicated that down-expression of miR-330-5p reversed the inhibitory effect of PCAT6 on NSCLC cell growth, migration, and invasion.

CONCLUSION

Our results reveal that lncRNA PCAT6 facilitates the proliferation, migration, and invasion of NSCLC cell via competitively binding to miR-330-5p.

摘要

背景

研究长链非编码RNA前列腺癌相关转录本6(PCAT6)在调节非小细胞肺癌(NSCLC)细胞生长和侵袭性中的作用。

方法

采用定量实时PCR检测法测定NSCLC组织和细胞系中PCAT6的水平。运用MTT法和集落形成试验探讨PCAT6对NSCLC细胞体外生长的影响。采用伤口愈合试验和Transwell试验分析PCAT6对NSCLC细胞迁移和侵袭的影响。利用生物信息学分析和荧光素酶报告基因试验证明miR-330-5p是PCAT6的靶标。通过集落形成试验、伤口愈合试验和Transwell侵袭试验证明PCAT6通过与miR-330-5p结合促进NSCLC细胞的生长、迁移和侵袭。最后,采用异种移植模型探讨PCAT6在NSCLC细胞体内肿瘤生长中的作用。

结果

与正常组织和非致瘤性支气管上皮细胞系BEAS-2B相比,PCAT6在NSCLC组织和细胞中高表达。PCAT6的下调显著降低了NSCLC细胞的增殖、迁移和侵袭能力。此外,PCAT6的下调显著提高了NSCLC细胞中miR-330-5p的水平。进一步的功能实验表明,miR-330-5p的下调逆转了PCAT6对NSCLC细胞生长、迁移和侵袭的抑制作用。

结论

我们的结果表明,长链非编码RNA PCAT6通过竞争性结合miR-330-5p促进NSCLC细胞的增殖、迁移和侵袭。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c46/6219114/247b64c9eee0/ott-11-7715Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c46/6219114/573e7eb00568/ott-11-7715Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c46/6219114/b820860968d6/ott-11-7715Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c46/6219114/81e74a33cdd2/ott-11-7715Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c46/6219114/4d13fa859692/ott-11-7715Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c46/6219114/247b64c9eee0/ott-11-7715Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c46/6219114/573e7eb00568/ott-11-7715Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c46/6219114/b820860968d6/ott-11-7715Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c46/6219114/81e74a33cdd2/ott-11-7715Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c46/6219114/4d13fa859692/ott-11-7715Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c46/6219114/247b64c9eee0/ott-11-7715Fig5.jpg

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