TACC3 promotes prostate cancer cell proliferation and restrains primary cilium formation

被引:25
作者
Qie, Yunkai [1 ]
Wang, Lin [1 ]
Du, E. [1 ]
Chen, Shuaiqi [2 ]
Lu, Chao [3 ]
Ding, Na [1 ]
Yang, Kuo [1 ]
Xu, Yong [1 ]
机构
[1] Tianjin Med Univ, Tianjin Inst Urol, Dept Urol, Hosp 2, Pingjiang Rd 23, Tianjin 300211, Peoples R China
[2] Xinxiang Med Univ, Dept Urol, Affiliated Hosp 1, Xinxiang 453100, Henan, Peoples R China
[3] Weifang Med Univ, Dept Reprod Med, Affiliated Hosp, Weifang 261031, Shandong, Peoples R China
基金
中国国家自然科学基金;
关键词
Prostate cancer; Primary cilia; TACC3; Filamin A; Meckelin; AURORA; KINASE; INHIBITION; ACTIVATION; CARCINOMA; PROTEINS; FAMILY;
D O I
10.1016/j.yexcr.2020.111952
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Although primary cilia abnormalities have been frequently observed in multiple cancers, including prostate cancer (PCa), the molecular mechanisms underlying primary ciliogenesis repression in PCa cells remain unclear. Transforming acidic coiled-coil protein-3 (TACC3), whose deregulation has been implicated in the pathogenesis of several types of cancer, is a key centrosomal protein that plays a crucial role in centrosome/microtubule dynamics, potentially impacting primary cilium generation. Here, we showed that TACC3 was markedly upregulated in PCa and that knockdown of TACC3 restrained tumorigenesis and tumor growth in vitro and in vivo. Additionally, we found that TACC3 interacts with filamin A, and elevated levels of TACC3 disrupted the interaction between filamin A and meckelin, thereby restraining primary cilium formation in PCa cells.
引用
收藏
页数:7
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