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

被引:37
作者
Zhang, Pei-pei [1 ]
Wang, Yi-qin [2 ]
Weng, Wei-wei [1 ]
Nie, Wei [3 ]
Wu, Yong [1 ]
Deng, Yu [1 ]
Wei, Ping [1 ]
Xu, Mi-die [1 ]
Wang, Chao-fu [4 ]
机构
[1] Fudan Univ, Shanghai Canc Ctr, Dept Pathol, 270 Dongan Rd, Shanghai 200032, Peoples R China
[2] Fudan Univ, Obstet & Gynecol Hosp, Dept Pathol, Shanghai, Peoples R China
[3] Second Mil Med Univ, Shanghai Changzheng Hosp, Dept Resp, Shanghai 200003, Peoples R China
[4] Shanghai Jiao Tong Univ, Rui Jin Hosp, Sch Med, Dept Pathol, 197 Rui Jin Er Rd, Shanghai 20025, Peoples R China
基金
中国国家自然科学基金;
关键词
Linc00152; lung adenocarcinoma; prognosis; proliferation; invasion; NONCODING RNA LINC00152; GASTRIC-CANCER; HEPATOCELLULAR-CARCINOMA; CLINICAL-SIGNIFICANCE; EXPRESSION; METASTASIS; PATHWAY;
D O I
10.7150/jca.18852
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:2042 / 2050
页数:9
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