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首页> 外文期刊>Journal of Cellular Physiology >LncRNA DGCR5 promotes lung adenocarcinoma (LUAD) progression via inhibiting hsa‐mir‐22‐3p
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LncRNA DGCR5 promotes lung adenocarcinoma (LUAD) progression via inhibiting hsa‐mir‐22‐3p

机译：LncRNA DGCR5促进肺腺癌(LUAD)进程通过抑制hsa必经米尔22应承担的3 p

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摘要

Long non‐coding RNAs (lncRNAs) serve critical roles in the pathogenesis of various cancers, including lung adenocarcinoma (LUAD). Herein, in this study, we aimed to investigate the biological and clinical significance of lncRNA DiGeorge syndrome critical region gene 5 (DGCR5) in LUAD. It was observed that DGCR5 was upregulated in LUAD tissues and LUAD cell lines. Inhibition of DGCR5 can prevent LUAD progression via playing anti‐apoptosis roles. Both mRNA expression and protein levels of BCL‐2 were increased by DGCR5 downregulation while reversely BAX was increased. Additionally, a novel microRNA target of DGCR5, hsa‐mir‐22‐3p was identified through bioinformatics search and confirmed by dual‐luciferase reporter system. Gain and loss‐of‐function studies were performed to verify whether DGCR5 exerts its biological functions through regulating hsa‐mir‐22‐3p in vitro. Overexpression of DGCR5 was able to reverse the tumor inhibitory effect of hsa‐mir‐22‐3p mimics. Furthermore, in vivo tests tumor xenografts were established to detect the function of DGCR5 in LUAD tumorigenesis. Downregulated DGCR5 expression was greatly associated with smaller tumor size, implying a favorable prognosis of LUAD patients. Taken these together, DGCR5 could be considered as a prognostic biomarker and therapeutic target in LUAD diagnosis and treatment.
机译：长非编码rna (lncRNAs)为关键角色在各种癌症的发病机制,包括肺腺癌(LUAD)。这项研究中,我们旨在调查lncRNA生物和临床意义迪格奥尔格综合征临界区基因5 (DGCR5)在LUAD。调节在LUAD组织和LUAD细胞系。抑制DGCR5可以防止LUAD进展通过玩抗细胞凋亡的作用。表达和蛋白质水平的BCL 2增加了,而相对地差别DGCR5对这些伯灵顿是增加。DGCR5,保险公司应承担的米尔22应承担的3 p被确认通过生物信息学搜索和确认双荧光素酶报告系统。功能丧失优先车道研究进行验证是否DGCR5施加它的生物功能通过调节hsa必经米尔22应承担的3 p体外。超表达DGCR5得以扭转肿瘤抑制作用的hsa米尔22应承担的3 p应承担的模仿。此外,体内测试肿瘤异种移植建立了检测DGCR5的函数LUAD肿瘤发生。表达非常小肿瘤大小,这意味着良好的预后LUAD病人。被视为一种预后生物标志物和在LUAD诊断和治疗目标治疗。

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