Research Papers:

CCDC34 is up-regulated in bladder cancer and regulates bladder cancer cell proliferation, apoptosis and migration

Yanqing Gong, Wei Qiu, Xianghui Ning, Xinyu Yang, Libo Liu, Zicheng Wang, Jian Lin, Xuesong Li and Yinglu Guo _

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Oncotarget. 2015; 6:25856-25867. https://doi.org/10.18632/oncotarget.4624

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Yanqing Gong1,2,3, Wei Qiu4, Xianghui Ning1,2, Xinyu Yang1,2,3, Libo Liu1,2,3, Zicheng Wang1,2, Jian Lin1,2,3, Xuesong Li1,2,3, Yinglu Guo1,2,3

1Department of Urology, Peking University First Hospital, Beijing 100034, China

2Institute of Urology, Peking University, Beijing 100034, China

3National Urological Cancer Center, Beijing 100034, China

4Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China

Correspondence to:

Yinglu Guo, e-mail: [email protected]

Xuesong Li, e-mail: [email protected]

Keywords: CCDC34, bladder cancer, siRNA, proliferation, migration

Received: May 21, 2015     Accepted: July 03, 2015     Published: July 16, 2015


The coiled coil is a superhelical structural protein motif involved in a diverse array of biological functions, and the abnormal expression of the coiled-coil domain containing proteins has a direct link with the phenotype of tumor cell migration, invasion and metastasis. The aim of this study was to investigate the critical role of Coiled-coil domain-containing protein 34 (CCDC34) in bladder carcinogenesis, which has never been reported to date. Here, we found CCDC34 expression was elevated in bladder cancer tissues and cell lines. The knockdown of CCDC34 via lentivirus-mediated siRNA significantly suppressed bladder cancer cells proliferation and migration, and induced cell cycle arrest at G2/M phase and increased apoptosis in vitro. In addition, CCDC34 knockdown suppressed bladder tumor growth in nude mice. Moreover, CCDC34 silencing decreased the phosphorylation of MEK, ERK1/2, JNK, p38 and Akt, and the expressions of c-Raf and c-Jun, indicating MAPK and AKT pathways (ERK/MAPK, p38/MAPK, JNK/MAPK and PI3K/Akt) might be involved in CCDC34 regulation of bladder cancer cell proliferation and migration. Our findings revealed for the first time a potential oncogenic role for CCDC34 in bladder carcinoma pathogenesis and it may serve as a biomarker or even a therapeutic target for bladder cancer.

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