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Tumour Biol. 2016 Sep;37(9):12855-12866. Epub 2016 Jul 23.

Overexpression of MYCN promotes proliferation of non-small cell lung cancer.

Liu K1, Wang S1,2,3, Liu Y4, Gu J5, Gu S6, Xu Z6, Zhang R5, Wang Z2, Ma H7, Chen Y3,6, Ji L8,9.

Author information

1
Department of Cardiothoracic Surgery, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
2
Department of Pathology, Medical School of Nantong University, Nantong, 226001, Jiangsu, China.
3
Jiangsu Province Key Laboratory for Inflammation and Molecular Target, Medical School of Nantong University, Nantong, 226001, Jiangsu, China.
4
Department of Pathology, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
5
Department of Respiratory, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
6
Department of Oncology, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
7
Department of Otorhinolaryngology, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
8
Department of Pathology, Medical School of Nantong University, Nantong, 226001, Jiangsu, China. liliji79@ntu.edu.cn.
9
Jiangsu Province Key Laboratory for Inflammation and Molecular Target, Medical School of Nantong University, Nantong, 226001, Jiangsu, China. liliji79@ntu.edu.cn.

Abstract

V-myc avian myelocytomatosis viral oncogene neuroblastoma derived homolog (MYCN) is an oncogene that is known amplified and overexpressed in different human malignancies including small cell lung cancer. However, the role of MYCN in non-small cell lung cancer (NSCLC) development remains elusive. In the present study, Western blot and immunohistochemistry assays demonstrated that MYCN was overexpressed in NSCLC tumor tissues and cell lines. In addition, immunohistochemistry analysis revealed that upregulation of MYCN expression was positively correlated with a more invasive tumor phenotype and poor prognosis. In vitro studies using serum starvation-refeeding experiment and MYCN-siRNA transfection assay demonstrated that MYCN expression promoted proliferation of NSCLC cells, while MYCN knockdown led to decreased cell growth resulted from growth arrest of cell cycle at G0/G1 phase. Furthermore, upregulation and knockdown of sex-determining region Y-box 2 (SRY) (SOX2), which was a well-known oncogene, confirmed that MYCN might be a downstream gene of the transcription factor SOX2. Collectively, our finding suggested that MYCN might contribute to the progression of NSCLC by enhancing cell proliferation, and that targeting MYCN might provide beneficial effects for the clinical therapy of NSCLC.

KEYWORDS:

Cell cycle; MYCN; NSCLC; Proliferation; SOX2

PMID:
27449038
DOI:
10.1007/s13277-016-5236-2
[Indexed for MEDLINE]

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