Research Papers:

CCDC106 promotes non-small cell lung cancer cell proliferation

Xiupeng Zhang, Qin Zheng, Chen Wang, Haijing Zhou, Guiyang Jiang, Yuan Miao, Yong Zhang, Yang Liu _, Qingchang Li, Xueshan Qiu and Enhua Wang

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Oncotarget. 2017; 8:26662-26670. https://doi.org/10.18632/oncotarget.15792

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Xiupeng Zhang1,2, Qin Zheng1,2, Chen Wang1,2, Haijing Zhou1,2, Guiyang Jiang1,2, Yuan Miao1,2, Yong Zhang3, Yang Liu1,2, Qingchang Li1,2, Xueshan Qiu1,2, Enhua Wang1,2

1Department of Pathology, College of Basic Medical Sciences, China Medical University, Shenyang, China

2Department of Pathology, First Affiliated Hospital, China Medical University, Shenyang, China

3Department of Pathology, Cancer Hospital of China Medical University, Shenyang, China

Correspondence to:

Yang Liu, email: [email protected]

Keywords: CCDC106, lung cancer, AKT signaling, cyclin A2, cyclin B1

Received: November 16, 2016     Accepted: February 16, 2017     Published: March 01, 2017


Coiled-coil domain containing (CCDC) family members enhance tumor cell proliferation, and high CCDC protein levels correlate with unfavorable prognoses. Limited research demonstrated that CCDC106 may promote the degradation of p53/TP53 protein and inhibit its transactivity. The present study demonstrated that CCDC106 expression correlates with advanced TNM stage (P = 0.008), positive regional lymph node metastasis (P < 0.001), and poor overall survival (P < 0.001) in 183 non-small cell lung cancer cases. A549 and H1299 cells were selected as representative of CCDC106-low and CCDC106-high expressing cell lines, respectively. CCDC106 overexpression promoted A549 cell proliferation and xenograft tumor growth in nude mice, while siRNA-mediated CCDC106 knockdown inhibited H1299 cell proliferation. CCDC106 promoted AKT phosphorylation and upregulated the cell cycle-regulating proteins Cyclin A2 and Cyclin B1. Cell proliferation promoted by CCDC106 via Cyclin A2 and Cyclin B1 was rescued by treatment with the AKT inhibitor, LY294002. Our studies revealed that CCDC106 is associated with non-small cell lung cancer progression and unfavorable prognosis. CCDC106 enhanced Cyclin A2 and Cyclin B1 expression and promoted A549 and H1299 cell proliferation, which depended on AKT signaling. These results suggest that CCDC106 may be a novel target for lung cancer treatment.

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