Linc00152 promotes Cancer Cell Proliferation and Invasion and Predicts Poor Prognosis in Lung adenocarcinoma.

Linc00152 promotes Cancer Cell Proliferation and Invasion and Predicts Poor Prognosis in Lung adenocarcinoma.
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Linc00152促进癌细胞增殖和侵袭并预测肺腺癌的不良预后

DOI:
10.7150/jca.18852
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发表时间:
2017
期刊:
影响因子:
3.9
通讯作者:
Wang CF
Wang CF
中科院分区:
医学3区
文献类型:
--
作者:
Zhang PP;Wang YQ;Weng WW;Nie W;Wu Y;Deng Y;Wei P;Xu MD;Wang CF

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背景:长链非编码RNA Linc00152刺激肿瘤进展。然而,其在肺腺癌中的临床意义和生物学功能尚不清楚。我们评估了Linc00152在肺腺癌中的表达及其与临床病理特征和患者生存的可能相关性,以揭示其在肿瘤进展和预后中的生物学作用。方法:对110对肺腺癌及邻近正常组织标本进行总RNA提取,并进行RT-qPCR。采用卡方检验分析计算病理参数与Linc00152 mRNA表达水平的相关性。采用Kaplan-Meier和Cox比例风险分析分析总生存率(OS)和无病生存率(DFS)。我们还检测了Linc00152过表达和敲低对体外细胞增殖、肿瘤细胞侵袭和迁移以及体内裸鼠异种移植和转移模型的潜在功能影响。结果:Linc00152在肺腺癌组织中的表达水平高于癌旁正常组织。Linc00152表达水平与淋巴结转移部位、远处转移及TNM分期密切相关。Kaplan-Meier分析提示,Linc00152高表达导致OS和DFS发生率显著降低,多因素分析显示,Linc00152是DFS和OS的独立危险因素。肺癌细胞中过表达Linc00152可促进肿瘤细胞增殖、侵袭和迁移。敲低Linc00152抑制细胞生长,抑制细胞侵袭和迁移。最后,在裸鼠模型中,Linc00152基因敲低抑制肺肿瘤生长和肿瘤转移。结论:我们的研究表明,Linc00152独立预测肺腺癌的不良预后并促进肿瘤进展。在未来的癌症药理学研究中,Linc00152是一个潜在的分子靶点。
Background: The long non-coding RNA Linc00152 stimulates tumor progression in cancer. However, its clinical significance and biological functions in lung adenocarcinoma remains unknown. We evaluate the expression of Linc00152 in lung adenocarcinoma and its possible correlation with clinicopathologic features and patient survival to reveal its biological effects in cancer progression and prognosis. Methods: Total RNA extraction was performed on 110 pairs of lung adenocarcinoma and adjacent normal tissue samples, and then RT-qPCR was conducted. Chi-square test analysis was used to calculate the correlation between pathological parameters and the Linc00152 mRNA levels. Kaplan-Meier and Cox proportional hazards analyses were used to analyze the overall survival (OS) and disease-free survival (DFS) rates. We also detected the potential functional effects of overexpression and knockdown of Linc00152 in vitro cell proliferation, tumor cell invasion and migration, as well as in vivo nude mouse xenograft and metastasis models. Results: The Linc00152 expression levels were higher in lung adenocarcinoma samples than in the adjacent normal tissues. Linc00152 expression levels tightly correlated with lymph node metastasis station, remote metastasis and TNM staging. The Kaplan-Meier analysis suggested that high Linc00152 expression caused significantly poorer OS and DFS rates, and a multivariate analysis revealed that Linc00152 was an independent risk factor for both DFS and OS. Overexpression of Linc00152 in lung cancer cells stimulated proliferation, tumor cell invasion and migration. Knockdown of Linc00152 inhibited cell growth and cell invasion and migration. Finally, Linc00152 knockdown inhibited lung tumor growth and tumor metastasis in nude mice models. Conclusions: Our study suggests that Linc00152 independently predicts poor prognosis and promotes tumor progression in lung adenocarcinoma. Linc00152 needs to be considered as a potential molecular target in future cancer pharmacology.
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DOI: 10.3892/or.2016.4758
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