Shen Zhiqing, Yu Xueping, Zheng Yijuan, Lai Xueping, Li Julan, Hong Yuxiang, Zhang Huatang, Chen Chunlin, Su Zhijun, Guo Ruyi
Department of Infectious Diseases, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou, China.
Onco Targets Ther. 2018 Feb 20;11:891-901. doi: 10.2147/OTT.S154754. eCollection 2018.
CDCA5 plays an important role in the development of various human cancers, but the associated mechanisms have not been investigated in hepatocellular carcinoma (HCC).
We evaluated expression levels and functions of CDCA5 in HCC and showed that CDCA5 is upregulated in HCC tissues compared with paired or unpaired normal liver tissues.
Increased CDCA5 expression in HCCs was significantly associated with shorter survival of patients. Knockdown of CDCA5 using lentivirus-mediated shRNA significantly inhibited cell proliferation and suppressed cell survival, as well as induced cell cycle arrest at the G2/M phase and cell apoptosis of HCC cells. The tumor suppression effects of CDCA5 knockdown were mediated by decreased expression of cyclin-dependent kinase 1 (CDK1) and CyclinB1, which were increased in HCC tissues comparing with adjacent normal liver tissues. Moreover, upregulation of CDCA5 was positively associated with increased CDK1 and CyclinB1 expression in HCC tissues.
The present data warrant consideration of CDCA5 as a prognostic biomarker and therapeutic target for HCC.
细胞分裂周期蛋白5（CDCA5）在多种人类癌症的发展中起重要作用，但尚未在肝细胞癌（HCC）中研究其相关机制。
我们评估了CDCA5在肝癌中的表达水平和功能，结果显示与配对或未配对的正常肝组织相比，CDCA5在肝癌组织中上调。
肝癌中CDCA5表达增加与患者生存期缩短显著相关。使用慢病毒介导的短发夹RNA（shRNA）敲低CDCA5可显著抑制细胞增殖、抑制细胞存活，并诱导肝癌细胞在G2/M期发生细胞周期阻滞和细胞凋亡。CDCA5敲低的肿瘤抑制作用是通过细胞周期蛋白依赖性激酶1（CDK1）和细胞周期蛋白B1（CyclinB1）表达降低介导的，与相邻正常肝组织相比，它们在肝癌组织中表达增加。此外，肝癌组织中CDCA5的上调与CDK1和CyclinB1表达增加呈正相关。
目前的数据值得将CDCA5视为肝癌的预后生物标志物和治疗靶点。
