Linc00467 promotes lung adenocarcinoma proliferation via sponging miR-20b-5p to activate CCNDI expression
Linc00467 promotes lung adenocarcinoma proliferation via sponging miR-20b-5p to activate CCNDI expression
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DOI：
10.2147/ott.s207748
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发表时间：
2019-01-01
影响因子：
4
通讯作者：
Xiong, Mengqing
中科院分区：
文献类型：
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作者：
Ding, Hao;Luo, Yuchuan;Xiong, Mengqing
背景：近年来，大量研究表明长链非编码RNA（lncRNA）在人类肿瘤中的作用。Linc 00467是一种新定义的lncRNA，据报道可促进神经母细胞瘤的细胞存活。然而，linc 00467在肺癌中的功能仍不清楚。材料和方法：我们分析了linc 00467的表达和生存数据来自癌症基因组Altas肺腺癌（LUAD）数据集以及在收集的LUAD组织。然后，我们沉默linc 00467在两个肺癌细胞系中使用小干扰RNA的表达，并探讨在体外和体内的细胞生长的影响linc 00467敲低。此外，我们发现了一个新的靶基因linc 00467，并阐明了其在肺癌细胞中的竞争性内源性RNA调控机制。结果：我们的数据表明linc 00467在LUAD组织中的表达升高，并与LUAD患者的总生存率相关。Linc 00467敲低导致肺癌细胞增殖率降低。结论：Linc 00467/miR-20 b-5 p/CCND 1信号通路可能为肺癌的治疗提供新的思路。
Background: Recently, numerous studies have demonstrated the emerging role of long non-coding RNAs (lncRNAs) in human cancers. Linc00467 is a newly defined lncRNA and was reported to promote cell survival in neuroblastoma. However, the function of linc00467 in lung cancer is still unclear.Material and methods: We analyzed linc00467 expression and survival data derived from The Cancer Genome Altas lung adenocarcinoma (LUAD) dataset as well as in collected LUAD tissues. Then, we silenced linc00467 expression in two lung cancer cell lines using small interfering RNAs and explored the effect of linc00467 knockdown on cell growth in vitro and in vivo. Moreover, we revealed a novel target gene of linc00467 and elucidated the underlying competitive endogenous RNA regulatory mechanism in lung cancer cells.Results: Our data suggested that linc00467 expression was elevated in LUAD tissues and correlated with overall survival of LUAD patients. Linc00467 knockdown resulted in reduced proliferation rate in lung cancer cells. Furthermore, we elucidated that linc00467 promoted CCND1 expression in lung cancer cells via functioning as a molecular sponge for miR-20b-5p.Conclusion: Linc00467/miR-20b-5p/CCND1 signaling pathway may provide new insights into lung cancer treatment.