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CCAT2是一种肺腺癌特异性长链非编码RNA,可促进非小细胞肺癌的侵袭。

CCAT2 is a lung adenocarcinoma-specific long non-coding RNA and promotes invasion of non-small cell lung cancer.

作者信息

Qiu Mantang, Xu Youtao, Yang Xin, Wang Jie, Hu Jingwen, Xu Lin, Yin Rong

机构信息

Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Nanjing Medical University Affiliated Cancer Hospital, Cancer Institute of Jiangsu Province, Nanjing, 210009, China.

出版信息

Tumour Biol. 2014 Jun;35(6):5375-80. doi: 10.1007/s13277-014-1700-z. Epub 2014 Feb 7.

Abstract

The prognosis of non-small cell lung cancer (NSCLC) is still poor, and it is necessary to identify effectively diagnostic and prognostic biomarkers for NSCLC. Recent evidence demonstrates that long non-coding RNA (lncRNA) is actively transcribed from human genome. Some lncRNAs show a time- or tissue-specific expression manner and play important roles in diverse biological processes. Additionally, various cancer-associated lncRNAs have been identified, such as metastasis-associated lung adenocarcinoma transcript 1 for lung cancer. Here, we characterized the expression profile of a novel lncRNA, colon cancer-associated transcript 2 (CCAT2), in lung cancer and found that CCAT2 was significantly over-expressed in NSCLC tissues compared with paired adjacent normal tissues, with an average up-regulation fold of 7.5. Intriguingly, over-expression of CCAT2 was significantly associated with lung adenocarcinoma (p=0.033) but not squamous cell cancer. Silencing CCAT2 by siRNA led to inhibition of proliferation and invasion in NSCLC cell lines in vitro. Additionally, CCAT2 combined with CEA could predict lymph node metastasis. Our findings indicate that CCAT2 is a lung adenocarcinoma-specific lncRNA and promotes invasion of NSCLC and highlight its potential as a biomarker for lymph node metastasis.

摘要

非小细胞肺癌(NSCLC)的预后仍然很差,因此有必要为NSCLC确定有效的诊断和预后生物标志物。最近的证据表明,长链非编码RNA(lncRNA)是从人类基因组中活跃转录而来的。一些lncRNAs表现出时间或组织特异性的表达方式,并在多种生物学过程中发挥重要作用。此外,已经鉴定出各种与癌症相关的lncRNAs,例如肺癌的转移相关肺腺癌转录本1。在此,我们对一种新型lncRNA——结肠癌相关转录本2(CCAT2)在肺癌中的表达谱进行了表征,发现与配对的相邻正常组织相比,CCAT2在NSCLC组织中显著过表达,平均上调倍数为7.5。有趣的是,CCAT2的过表达与肺腺癌显著相关(p = 0.033),但与鳞状细胞癌无关。通过siRNA沉默CCAT2可导致体外NSCLC细胞系的增殖和侵袭受到抑制。此外,CCAT2与癌胚抗原(CEA)联合可预测淋巴结转移。我们的研究结果表明,CCAT2是一种肺腺癌特异性lncRNA,可促进NSCLC的侵袭,并突出了其作为淋巴结转移生物标志物的潜力。

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