LncRNA MEG3 inhibits the progression of prostate cancer by modulating miR-9-5p/QKI-5 axis
LncRNA MEG3 inhibits the progression of prostate cancer by modulating miR-9-5p/QKI-5 axis
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DOI：
10.1111/jcmm.13658
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发表时间：
2019-01-01
影响因子：
5.3
通讯作者：
Xi, Xiaoqing
中科院分区：
文献类型：
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作者：
Wu, Meng;Huang, Yawei;Xi, Xiaoqing
本研究旨在检测lncRNA MEG 3在前列腺癌中的作用。通过微阵列分析筛选前列腺癌的异常lncRNA表达谱。采用qRT-PCR和Western blot检测lncRNA MEG 3、miR-9- 5 p和QKI-5的表达水平。利用荧光素酶报告基因检测技术验证了这些分子之间的相互作用关系。分别采用CCK-8法、创伤愈合法、transwell法和流式细胞术检测细胞增殖、迁移、侵袭能力和凋亡情况。LncRNA MEG 3是前列腺癌组织和细胞中下调的lncRNA，可抑制miR-9- 5 p的表达，而miR-9- 5 p下调QKI-5的表达。MEG 3和QKI-5过表达可有效降低前列腺癌细胞的增殖、迁移和侵袭能力，增加细胞凋亡率。相反，miR-9- 5 p模拟物在前列腺癌细胞中呈现相反的趋势。此外，MEG 3在体内抑制肿瘤生长并上调QKI-5的表达。LncRNA MEG 3在前列腺癌中是一种下调的lncRNA，影响细胞增殖、迁移和侵袭能力以及细胞凋亡率，这种调节依赖于对miR-9- 5 p及其靶基因QKI-5的调控。
This study was designed to detecting the influences of lncRNA MEG3 in prostate cancer. Aberrant lncRNAs expression profiles of prostate cancer were screened by microarray analysis. The qRT-PCR and Western blot were employed to investigating the expression levels of lncRNA MEG3, miR-9-5p and QKI-5. The luciferase reporter assay was utilized to testifying the interactions relationship among these molecules. Applying CCK-8 assay, wound healing assay, transwell assay and flow cytometry in turn, the cell proliferation, migration and invasion abilities as well as apoptosis were measured respectively. LncRNA MEG3 was a down-regulated lncRNA in prostate cancer tissues and cells and could inhibit the expression of miR-9-5p, whereas miR-9-5p down-regulated QKI-5 expression. Overexpressed MEG3 and QKI-5 could decrease the abilities of proliferation, migration and invasion in prostate cancer cells effectively and increased the apoptosis rate. On the contrary, miR-9-5p mimics presented an opposite tendency in prostate cancer cells. Furthermore, MEG3 inhibited tumour growth and up-regulated expression of QKI-5 in vivo. LncRNA MEG3 was a down-regulated lncRNA in prostate cancer and impacted the abilities of cell proliferation, migration and invasion, and cell apoptosis rate, this regulation relied on regulating miR-9-5p and its targeting gene QKI-5.