Department of Cardiothoracic Surgery, Affiliated Hospital of Guangdong Medical University, Zhanjiang, P.R. China.
Eur Rev Med Pharmacol Sci. 2020 Mar;24(6):3166-3173. doi: 10.26355/eurrev_202003_20683.
To verify that miR-92b inhibits proliferation and invasion of lung cancer by targeting EZH2.
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.
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).
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.
通过靶向抑制 EZH2 来验证 miR-92b 抑制肺癌的增殖和侵袭。
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。
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)。
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。