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LncRNA GMDS-AS1 inhibits lung adenocarcinoma development by regulating miR-96-5p/CYLD signaling.
Cancer Medicine ( IF 4 ) Pub Date : 2019-12-20 , DOI: 10.1002/cam4.2776
Ming Zhao 1 , Xiao-Feng Xin 1 , Jian-Ya Zhang 1 , Wei Dai 1 , Tang-Feng Lv 1 , Yong Song 1
Affiliation  

According to the global cancer statistic, lung cancer is one of the most dangerous tumors, which poses a serious threat to human health. Exploration the mechanism of lung cancer and new targeted therapeutic measures is always the hot topic. Long noncoding RNA (lncRNA) is an important factor affecting the development of tumors. However, the research on the mechanism of lncRNA in the progress of lung cancer needs to be further expanded. In this study, we found that the expression of lncRNA GMDS-AS1 was significantly reduced in lung adenocarcinoma (LUAD) tissues and cells. Upregulated GMDS-AS1 can significantly inhibit the proliferation of LUAD cells and promote cell apoptosis in vitro and in vivo. The results indicate that GMDS-AS1 acts as a tumor suppressor gene to affect the development of LUAD. Further studies revealed that GMDS-AS1 is a target gene of miR-96-5p, and GMDS-AS1 regulates proliferation and apoptosis of LUAD cells in association with miR-96-5p. In addition, we also confirmed that CYLD lysine 63 deubiquitinase (CYLD) is also a target gene of miR-96-5p. Through various validations, we confirmed that GMDS-AS1 can act as a ceRNA to upregulate the expression of CYLD by sponging miR-96-5p. Moreover, the intervention of GMDS-AS1/miR-96-5p/CYLD network can regulate the proliferation and apoptosis of LUAD cells. In this study, we revealed that the GMDS-AS1/miR-96-5p/CYLD network based on ceRNA mechanism plays an important role in the development of LUAD and provides a new direction and theoretical basis for targeted therapy of LUAD.

中文翻译:

LncRNA GMDS-AS1通过调节miR-96-5p / CYLD信号传导抑制肺腺癌的发展。

根据全球癌症统计数据,肺癌是最危险的肿瘤之一,对人类健康构成了严重威胁。探索肺癌的机制和新的靶向治疗措施一直是热门话题。长非编码RNA(lncRNA)是影响肿瘤发展的重要因素。然而,有关lncRNA在肺癌进展中机制的研究尚需进一步扩展。在这项研究中,我们发现lncRNA GMDS-AS1在肺腺癌(LUAD)组织和细胞中的表达明显降低。GMDS-AS1的上调可以显着抑制LUAD细胞的增殖,并在体内外促进细胞凋亡。结果表明,GMDS-AS1是一个肿瘤抑制基因,可影响LUAD的发育。进一步的研究表明,GMDS-AS1是miR-96-5p的靶基因,而GMDS-AS1与miR-96-5p相关联地调节LUAD细胞的增殖和凋亡。此外,我们还证实CYLD赖氨酸63去泛素酶(CYLD)也是miR-96-5p的靶基因。通过各种验证,我们证实了GMDS-AS1可以作为ceRNA,通过使miR-96-5p变海绵来上调CYLD的表达。此外,GMDS-AS1 / miR-96-5p / CYLD网络的干预可以调节LUAD细胞的增殖和凋亡。在这项研究中,我们揭示了基于ceRNA机制的GMDS-AS1 / miR-96-5p / CYLD网络在LUAD的发展中起着重要作用,并为LUAD的靶向治疗提供了新的方向和理论基础。GMDS-AS1与miR-96-5p共同调控LUAD细胞的增殖和凋亡。此外,我们还证实CYLD赖氨酸63去泛素酶(CYLD)也是miR-96-5p的靶基因。通过各种验证,我们证实了GMDS-AS1可以作为ceRNA,通过使miR-96-5p变海绵来上调CYLD的表达。此外,GMDS-AS1 / miR-96-5p / CYLD网络的干预可以调节LUAD细胞的增殖和凋亡。在这项研究中,我们揭示了基于ceRNA机制的GMDS-AS1 / miR-96-5p / CYLD网络在LUAD的发展中起着重要作用,并为LUAD的靶向治疗提供了新的方向和理论基础。GMDS-AS1与miR-96-5p共同调控LUAD细胞的增殖和凋亡。此外,我们还证实CYLD赖氨酸63去泛素酶(CYLD)也是miR-96-5p的靶基因。通过各种验证,我们证实了GMDS-AS1可以作为ceRNA,通过使miR-96-5p变海绵来上调CYLD的表达。此外,GMDS-AS1 / miR-96-5p / CYLD网络的干预可以调节LUAD细胞的增殖和凋亡。在这项研究中,我们揭示了基于ceRNA机制的GMDS-AS1 / miR-96-5p / CYLD网络在LUAD的发展中起着重要作用,并为LUAD的靶向治疗提供了新的方向和理论基础。我们证实,GMDS-AS1可以作为ceRNA,通过使miR-96-5p变海绵来上调CYLD的表达。此外,GMDS-AS1 / miR-96-5p / CYLD网络的干预可以调节LUAD细胞的增殖和凋亡。在这项研究中,我们揭示了基于ceRNA机制的GMDS-AS1 / miR-96-5p / CYLD网络在LUAD的发展中起着重要作用,并为LUAD的靶向治疗提供了新的方向和理论基础。我们证实,GMDS-AS1可以作为ceRNA,通过使miR-96-5p变海绵来上调CYLD的表达。此外,GMDS-AS1 / miR-96-5p / CYLD网络的干预可以调节LUAD细胞的增殖和凋亡。在这项研究中,我们揭示了基于ceRNA机制的GMDS-AS1 / miR-96-5p / CYLD网络在LUAD的发展中起着重要作用,并为LUAD的靶向治疗提供了新的方向和理论基础。
更新日期:2019-12-21
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