Oncotarget

Research Papers:

CDCA2 promotes lung adenocarcinoma cell proliferation and predicts poor survival in lung adenocarcinoma patients

Run Shi, Chunrong Zhang, Yaqin Wu, Xin Wang, Qi Sun, Jing Sun, Wenjie Xia, Gaochao Dong, Anpeng Wang, Feng Jiang and Lin Xu _

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Oncotarget. 2017; 8:19768-19779. https://doi.org/10.18632/oncotarget.15519

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Abstract

Run Shi1,2,4,*, Chunrong Zhang1,4,6,*, Yaqin Wu1,4,*, Xin Wang1,2,4, Qi Sun5, Jing Sun3, Wenjie Xia1,2,4, Gaochao Dong1, Anpeng Wang1,2,4, Feng Jiang1,2, Lin Xu1,2

1Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Cancer Institute of Jiangsu Province, Jiangsu, China

2Department of Thoracic Surgery, Affiliated Cancer Hospital, Nanjing Medical University, Jiangsu, China

3The First Clinical College of Nanjing Medical University, Nanjing, China

4The Fourth Clinical College of Nanjing Medical University, Nanjing, China

5Department of Cardiothoracic Surgery at Jinling Hospital, Southern Medical University, Nanjing, China

6Department of Thoracic Surgery, Nantong Tumor Hospital, Jiangsu, China

*These authors contributed equally to this work

Correspondence to:

Feng Jiang, email: [email protected]

Lin Xu, email: [email protected]

Keywords: CDCA2, lung adenocarcinoma, TCGA, proliferation, prognosis

Received: July 10, 2016     Accepted: January 10, 2017     Published: February 19, 2017

ABSTRACT

Cell division cycle associated 2(CDCA2) is overexpressed in neuroblastoma and oral squamous cell carcinoma, and its overexpression positively correlates to tumor progression. However, the biological and clinical significance of CDCA2 in lung adenocarcinoma(LAC) has never been investigated. We determined the expression profile and clinical significance of CDCA2 using The Cancer Genome Atlas(TCGA) and tissue microarray(TMA). Furthermore, we explored the biological function of CDCA2 both in vitro and in vivo. A great upregulation of CDCA2 was observed in LAC tissues compared with adjacent normal tissues. Importantly, Cox regression analysis indicated that high level of CDCA2 was an independent risk factor for overall survival(OS) in LAC patients (TCGA: HR = 1.720, p = 0.004; TMA: HR = 1.971, p = 0.023). Inhibition of CDCA2 suppressed the proliferation of LAC cells via G1 phase arrest by downregulating cyclin E1(CCNE1), while overexpression of CDCA2 promoted LAC cells proliferation by upregulating CCNE1. Moreover, the oncogenic activity of CDCA2 was also confirmed in vivo. In conclusion, CDCA2 promotes proliferation of LAC cells and predicts poor prognosis in LAC patients. CDCA2 might play a significant role in LAC progression.


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