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Long non-coding RNA NEAT1 promotes non-small cell lung cancer progression through regulation of miR-377-3p-E2F3 pathway

Chengcao Sun _, Shujun Li, Feng Zhang, Yongyong Xi, Liang Wang, Yongyi Bi and Dejia Li

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Oncotarget. 2016; 7:51784-51814. https://doi.org/10.18632/oncotarget.10108

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Chengcao Sun1, Shujun Li1,2, Feng Zhang1, Yongyong Xi1, Liang Wang1, Yongyi Bi1, Dejia Li1

1Department of Occupational and Environmental Health, School of Public Health, Wuhan University, Wuhan, P. R. China

2Wuhan Hospital for the Prevention and Treatment of Occupational Diseases, Wuhan, P. R. China

Correspondence to:

Dejia Li, email: [email protected]

Keywords: long non-coding RNA NEAT1 (lncRNA NEAT1), hsa-miRNA-377-3p (miR-377-3p), E2F3, non-small cell lung cancer (NSCLC), tumorigenesis

Received: February 16, 2016    Accepted: May 05, 2016    Published: June 16, 2016


Recently, the long non-coding RNA (lncRNA) NEAT1 has been identified as an oncogenic gene in multiple cancer types and elevated expression of NEAT1 was tightly linked to tumorigenesis and cancer progression. However, the molecular basis for this observation has not been characterized in progression of non-small cell lung cancer (NSCLC). In our studies, we identified NEAT1 was highly expressed in patients with NSCLC and was a novel regulator of NSCLC progression. Patients whose tumors had high NEAT1 expression had a shorter overall survival than patients whose tumors had low NEAT1 expression. Further, NEAT1 significantly accelerates NSCLC cell growth and metastasis in vitro and tumor growth in vivo. Additionally, by using bioinformatics study and RNA pull down combined with luciferase reporter assays, we demonstrated that NEAT1 functioned as a competing endogenous RNA (ceRNA) for hsa-miR-377-3p, antagonized its functions and led to the de-repression of its endogenous targets E2F3, which was a core oncogene in promoting NSCLC progression. Taken together, these observations imply that the NEAT1 modulated the expression of E2F3 gene by acting as a ceRNA, which may build up the missing link between the regulatory miRNA network and NSCLC progression.

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