miR-30d-5p通过靶向DBF4抑制肺鳞状细胞癌的增殖、迁移和侵袭。

IF 1.2 4区 环境科学与生态学 Q4 ENVIRONMENTAL SCIENCES Journal of Environmental Science and Health Part C-Toxicology and Carcinogenesis Pub Date : 2021-01-01 Epub Date: 2021-06-24 DOI:10.1080/26896583.2021.1926855
Yitian Qi, Yi Hou, Liangchen Qi
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引用次数: 8

摘要

目的:本研究旨在探讨miR-30d-5p通过靶向DBF4调控肺鳞状细胞癌(LUSC)发生发展的机制。方法:采用生物信息学方法对LUSC组织芯片中差异表达基因进行分析。采用qRT-PCR检测miR-30d-5p和DBF4 mRNA在正常人支气管上皮细胞和LUSC细胞中的表达。CCK-8检测LUSC细胞活性。采用创面愈合实验检测LUSC细胞的迁移能力。采用Transwell检测侵入能力。采用双荧光素酶报告基因法检测miR-30d-5p与DBF4的靶向关系。Western blot检测上皮-间质转化(epithelial-mesenchymal transition, EMT)相关标记分子的蛋白表达。结果:本研究发现,miR-30d-5p在LUSC细胞系中的表达明显低于正常人支气管上皮细胞系,与DBF4的表达相反。双荧光素酶报告基因实验证实miR-30d-5p可靶向DBF4,过表达miR-30d-5p可下调DBF4的表达。过表达DBF4可促进LUSC的增殖、迁移、侵袭和EMT,而过表达miR-30d-5p可减弱DBF4对癌细胞的促进作用。结论:miR-30d-5p下调DBF4的表达,调控LUSC的发生发展。
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miR-30d-5p represses the proliferation, migration, and invasion of lung squamous cell carcinoma via targeting DBF4.

Objective: This study aims to explore the mechanism of miR-30d-5p in regulating the development of lung squamous cell carcinoma (LUSC) via targeting DBF4.

Methods: Bioinformatics methods were employed to analyze the differentially expressed genes in LUSC tissue microarray. qRT-PCR was employed to detect the expression of miR-30d-5p and DBF4 mRNA in normal human bronchial epithelial cells and LUSC cells. CCK-8 was used to detect LUSC cell activity. Wound healing assay was employed to detect the migratory ability of LUSC cells. Transwell was employed to detect invasive ability. Dual-luciferase reporter assay was used to detect the targeting relationship between miR-30d-5p and DBF4. Western blot was used to detect the protein expression of marker molecules associated with epithelial-mesenchymal transition (EMT).

Results: In this study, the expression of miR-30d-5p in LUSC cell lines was found to be obviously low compared with that in normal human bronchial epithelial cell line, which was opposite to the expression of DBF4. Dual-luciferase reporter assay verified that miR-30d-5p could target DBF4 and the overexpression of miR-30d-5p downregulated the expression of DBF4. Overexpression of DBF4 promoted the proliferation, migration, invasion, and EMT of LUSC, whereas over-expression of miR-30d-5p could weaken the promotion of DBF4 on cancer cells.

Conclusion: miR-30d-5p downregulates the expression of DBF4 to regulate the development of LUSC.

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