Long noncoding RNA CAR10 promotes lung adenocarcinoma metastasis via miR-203/30/SNAI axis
Long noncoding RNA CAR10 promotes lung adenocarcinoma metastasis via miR-203/30/SNAI axis
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长非编码RNA CAR10通过miR-203/30/SNAI轴促进肺腺癌转移
DOI：
10.1038/s41388-018-0645-x
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发表时间：
2019-04-18
期刊：
影响因子：
8
通讯作者：
Li, Zheng
中科院分区：
文献类型：
--
作者：
Ge, Xiaolu;Li, Gui-yuan;Li, Zheng
长链非编码RNA（lncRNA）在肺腺癌（LUAD）转移中起重要作用。在这里，我们发现lncRNA染色质相关RNA 10（CAR 10）在LUAD患者的肿瘤组织中上调，并在体外和体内增强肿瘤转移。从机制上讲，CAR 10通过直接与miR-30和miR-203结合，然后调节SNAH和SNAI 2的表达，诱导上皮向间充质转化（EMT）。CAR 10过表达与LUAD患者的不良预后呈正相关，而CAR 10和SNAI的过表达与更差的临床结局相关。总之，CAR 10/miR-30/203/SNAI轴是LUAD的新的和潜在的治疗靶点。
Long noncoding RNAs (lncRNAs) play an important role in lung adenocarcinoma (LUAD) metastasis. Here, we found that lncRNA chromatin-associated RNA 10 (CAR10) was upregulated in the tumor tissue of patients with LUAD and enhanced tumor metastasis in vitro and in vivo. Mechanistically, CAR10 induced epithelial-to-mesenchymal transition (EMT) by directly binding with miR-30 and miR-203 and then regulating the expression of SNAH and SNAI2. CAR10 overexpression was positively correlated with a poor prognosis in LUAD patients, whereas overexpression of both CAR10 and SNAI was correlated with even worse clinical outcomes. In conclusion, the CAR10/miR-30/203/SNAI axis is a novel and potential therapeutic target for LUAD.