Targeting of CCN2 suppresses tumor progression and improves chemo-sensitivity in urothelial bladder cancer
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Xiaojing Wang1,*, Tianyuan Xu1,*, Fengbin Gao1, Hongchao He1, Yu Zhu1 and Zhoujun Shen1,2
1Department of Urology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China
2Department of Urology, Huashan Hospital, Fudan University, Shanghai, China
*These authors have contributed equally to this work
Zhoujun Shen, email: [email protected]
Yu Zhu, email: [email protected]
Keywords: CCN2, bladder cancer, chemotherapy, mitomycin C
Received: April 15, 2017 Accepted: July 19, 2017 Published: August 07, 2017
Urothelial bladder cancer (UBC) is the most common urinary neoplasm in China. CCN family protein 2 (CCN2), a cysteine-rich matricellular protein, is abnormally expressed in several cancer types and involved in tumor progression or chemo-resistance. However, detailed expression patterns and effects of CCN2 in UBC still remain unknown. We found that down-regulation of CCN2 suppressed proliferation, migration and invasion of UBC cells in vitro and targeting of CCN2 decelerated xenograft growth in vivo. When treated with mitomycin C (MMC), CCN2-scilencing UBC cells showed lower survival and higher apoptotic rates and these effects were probably mediated via inactivation of Akt and Erk pathways. We also demonstrated the clinical significance of CCN2 expression, which was higher in UBC tissues and associated with advanced tumor stage and high pathologic grade. Taken together, our data suggest that CCN2 is an oncogene in UBC and might serve as a matricellular target for improving chemotherapeutic efficacy.
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