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长链非编码RNA CCAT1的过表达通过上皮-间质转化促进肺腺癌转移。

Overexpression of the long noncoding RNA CCAT1 promotes metastasis via epithelial-to-mesenchymal transition in lung adenocarcinoma.

作者信息

Lin Heping, Cheng Wei, Yan Hanhan, Zhang Xiaodiao

机构信息

Department of Respiratory Medicine, The Third Affiliated Hospital of Wenzhou Medical University, Rui'an, Wenzhou, Zhejiang 325200, P.R. China.

出版信息

Oncol Lett. 2018 Aug;16(2):1809-1814. doi: 10.3892/ol.2018.8813. Epub 2018 May 25.

Abstract

The long noncoding RNA (lncRNA) colon cancer-associated transcript 1 (CCAT1) has been identified as an oncogene in multiple types of human malignancy, and the aberrant expression of CCAT1 has been associated with the tumorigenesis and progression of cancer. However, the underlying mechanism of how CCAT1 affects malignant behaviors in lung adenocarcinoma cells remains unknown. In the current study, the expression of CCAT1 was identified to be increased in lung adenocarcinoma tissues (n=96) by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and its expression level was associated with epidermal growth factor receptor (EGFR) expression (P=0.011), lymphatic metastasis (P=0.003) and tumor node metastasis (TNM) stage (P=0.003). , by using Transwell assays, the overexpression of CCAT1 was demonstrated to promote the migration and invasion of H358 lung adenocarcinoma cells; while downregulation of CCAT1 expression inhibited H1650 cell migration and invasion. Furthermore, western blot analysis indicated that aberrant CCAT1 expression may induce epithelial-to-mesenchymal transition (EMT) by regulating the expression levels of EMT markers (E-cadherin, N-cadherin and vimentin). In conclusion, these results indicate that CCAT1 is able to promote the metastasis of lung adenocarcinoma cells by inducing EMT.

摘要

长链非编码RNA(lncRNA)结肠癌相关转录本1(CCAT1)已被确定为多种人类恶性肿瘤中的一种癌基因,CCAT1的异常表达与癌症的发生和发展有关。然而,CCAT1如何影响肺腺癌细胞恶性行为的潜在机制仍不清楚。在本研究中,通过逆转录定量聚合酶链反应(RT-qPCR)确定CCAT1在肺腺癌组织(n = 96)中的表达增加,其表达水平与表皮生长因子受体(EGFR)表达(P = 0.011)、淋巴转移(P = 0.003)和肿瘤淋巴结转移(TNM)分期(P = 0.003)相关。此外,通过Transwell实验证明,CCAT1的过表达促进了H358肺腺癌细胞的迁移和侵袭;而CCAT1表达下调则抑制了H1650细胞的迁移和侵袭。此外,蛋白质印迹分析表明,CCAT1的异常表达可能通过调节上皮-间质转化(EMT)标志物(E-钙黏蛋白、N-钙黏蛋白和波形蛋白)的表达水平来诱导EMT。总之,这些结果表明CCAT1能够通过诱导EMT促进肺腺癌细胞的转移。

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