High expression of N-myc (and STAT) interactor predicts poor prognosis and promotes tumor growth in human glioblastoma
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Delong Meng1,*, Yuanyuan Chen1,*, Dapeng Yun1, Yingjie Zhao1, Jingkun Wang1, Tao Xu2, Xiaoying Li1, Yuqi Wang1, Li Yuan1, Ruochuan Sun3, Xiao Song1, Cong Huai1, Lingna Hu1, Song Yang3, Taishan Min1, Juxiang Chen2, Hongyan Chen1 and Daru Lu1
1 State Key Laboratory of Genetic Engineering and MOE Key Laboratory of Contemporary Anthropology, Collaborative Innovation Center for Genetics and Development, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai, China
2 Department of Neurosurgery, Shanghai Institute of Neurosurgery, Changzheng Hospital, Second Military Medical University, Shanghai, China
3 The Eighth Department of General Surgery and Department of Pathology, The First Affiliated Hospital of Anhui Medical University, Hefei, China
* These authors contributed equally to this work
Daru Lu, email:
Hongyan Chen, email:
Keywords: NMI, glioblastoma, prognosis, immunohistochemistry, TCGA
Received: September 09, 2014 Accepted: December 25, 2014 Published: December 30, 2014
Glioma is the most malignant brain tumor and glioblastoma (GBM) is the most aggressive type. The involvement of N-myc (and STAT) interactor (NMI) in tumorigenesis was sporadically reported but far from elucidation. This study aims to investigate roles of NMI in human glioma. Three independent cohorts, the Chinese tissue microarray (TMA) cohort (N = 209), the Repository for Molecular Brain Neoplasia Data (Rembrandt) cohort (N = 371) and The Cancer Genome Atlas (TCGA) cohort (N = 528 or 396) were employed. Transcriptional or protein levels of NMI expression were significantly increased according to tumor grade in all three cohorts. High expression of NMI predicted significantly unfavorable clinical outcome for GBM patients, which was further determined as an independent prognostic factor. Additionally, expression and prognostic value of NMI were associated with molecular features of GBM including PTEN deletion and EGFR amplification in TCGA cohort. Furthermore, overexpression or depletion of NMI revealed its regulation on G1/S progression and cell proliferation (both in vitro and in vivo), and this effect was partially dependent on STAT1, which interacted with and was regulated by NMI. These data demonstrate that NMI may serve as a novel prognostic biomarker and a potential therapeutic target for glioblastoma.
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