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miR-92b 通过靶向 EZH2 抑制肺癌的增殖和侵袭。

MiR-92b inhibits proliferation and invasion of lung cancer by targeting EZH2.

机构信息

Department of Cardiothoracic Surgery, Affiliated Hospital of Guangdong Medical University, Zhanjiang, P.R. China.

出版信息

Eur Rev Med Pharmacol Sci. 2020 Mar;24(6):3166-3173. doi: 10.26355/eurrev_202003_20683.

Abstract

OBJECTIVE

To verify that miR-92b inhibits proliferation and invasion of lung cancer by targeting EZH2.

MATERIALS AND METHODS

The expression levels of miR-92b and EZH2 in human bronchial epithelial cell line BEAS-2B and human lung cancer cell line (A549, NCI-H23, NCI-H358, NCI-H1975, PC-9) were detected, and miR-92b mimic, sh-EZH2 expression vector, and plasmid blank vector (blank group) were constructed. Blank group, miR-92b mimic, miR-92b mimic+sh-EZH2 group (combined group) were set up, MTT and transwell were used to detect the proliferation and invasion ability of A549 and NCI-H23 cells, and fluorescein report verified the regulatory relationship of miR-92b to EZH2.

RESULTS

The expression level of miR-92b in A549, NCI-H23, NCI-H358, NCI-H1975, and PC-9 cells was lower than that in BEAS-2B cells (p<0.05). The expression level of EZH2 was higher than that of BEAS-2B cells (p<0.05). A549 and NCI-H23 cells were selected for transfection. After that, the expression level of miR-92 in miR-92b mimic, combined group A549 and NCI-H23 cells was higher than that in blank group (p<0.05), and miR-92b mimic had no difference with joint group (p>0.05). The expression level of EZH2 in cells of miR-92b mimic, blank group A549, and NCI-H23 was lower than that of combined group (p<0.05), and miR-92b mimic was lower than that of blank group (p<0.05). After the overexpression of miR-92b, pmirGLO-EZH2-3'UT Wt luciferase activity decreased significantly (p<0.05) but had no effect on pmirGLO-EZH2-3'UTR Mut Luciferase activity (p>0.05). Cell proliferation ability and invasion ability of A549 cells and NCI-H23 cells in miR-92b mimic group were lower than those in blank group (p<0.05), while those in combined group were higher than those in miR-92b mimic group (p<0.05).

CONCLUSIONS

MiR-92b inhibits proliferation and invasion of lung cancer cells through targeted inhibition of EZH2, which is a potential target for future treatment of lung cancer.

摘要

目的

通过靶向抑制 EZH2 来验证 miR-92b 抑制肺癌的增殖和侵袭。

材料和方法

检测人支气管上皮细胞系 BEAS-2B 和人肺癌细胞系(A549、NCI-H23、NCI-H358、NCI-H1975、PC-9)中 miR-92b 和 EZH2 的表达水平,并构建 miR-92b 模拟物、sh-EZH2 表达载体和质粒空白载体(空白组)。设置空白组、miR-92b 模拟物组、miR-92b 模拟物+sh-EZH2 组(联合组),MTT 和 Transwell 检测 A549 和 NCI-H23 细胞的增殖和侵袭能力,荧光素酶报告验证 miR-92b 对 EZH2 的调控关系。

结果

A549、NCI-H23、NCI-H358、NCI-H1975 和 PC-9 细胞中 miR-92b 的表达水平低于 BEAS-2B 细胞(p<0.05)。EZH2 的表达水平高于 BEAS-2B 细胞(p<0.05)。选择 A549 和 NCI-H23 细胞进行转染。之后,miR-92b 模拟物、联合组 A549 和 NCI-H23 细胞中 miR-92 的表达水平高于空白组(p<0.05),而联合组与 miR-92b 模拟物组无差异(p>0.05)。miR-92b 模拟物、空白组 A549 和 NCI-H23 细胞中 EZH2 的表达水平低于联合组(p<0.05),而 miR-92b 模拟物低于空白组(p<0.05)。miR-92b 过表达后,pmirGLO-EZH2-3'UTR Wt 荧光素酶活性显著降低(p<0.05),但对 pmirGLO-EZH2-3'UTR Mut 荧光素酶活性无影响(p>0.05)。A549 细胞和 NCI-H23 细胞中 miR-92b 模拟物组的细胞增殖能力和侵袭能力低于空白组(p<0.05),而联合组高于 miR-92b 模拟物组(p<0.05)。

结论

miR-92b 通过靶向抑制 EZH2 抑制肺癌细胞的增殖和侵袭,这可能成为未来治疗肺癌的潜在靶点。

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