Targeting of CCN2 suppresses tumor progression and improves chemo-sensitivity in urothelial bladder cancer

被引:8
作者
Wang, Xiaojing [1 ]
Xu, Tianyuan [1 ]
Gao, Fengbin [1 ]
He, Hongchao [1 ]
Zhu, Yu [1 ]
Shen, Zhoujun [1 ,2 ]
机构
[1] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Urol, Shanghai, Peoples R China
[2] Fudan Univ, Huashan Hosp, Dept Urol, Shanghai, Peoples R China
基金
中国国家自然科学基金;
关键词
CCN2; bladder cancer; chemotherapy; mitomycin C; TISSUE GROWTH-FACTOR; FACTOR CTGF/CCN2; DRUG-RESISTANCE; BREAST-CANCER; EXPRESSION; CTGF; CELLS; DIFFERENTIATION; OSTEOSARCOMA; METASTASIS;
D O I
10.18632/oncotarget.19987
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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 chemoresistance. 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.
引用
收藏
页码:66316 / 66327
页数:12
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