期刊
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
卷 15, 期 7, 页码 1488-1499出版社
IVYSPRING INT PUBL
DOI: 10.7150/ijbs.32718
关键词
TRIP13; Tumorigenesis; Bladder cancer; EGFR
资金
- National Natural Science Foundation of China [81672519, 8137273, 81172437]
- Natural Science Foundation Project of Gansu Province [1606RJZA044]
- Cuiying Scientific and Technological Innovation Program of Lanzhou University Second Hospital [CY2017-QN15]
Thyroid hormone receptor interactor 13 (TRIP13) is a crucial regulator of the spindle apparatus checkpoint and double-stranded break repair. The abnormal expression of TRIP13 was recently found in several human cancers, whereas the role of TRIP13 in the development of bladder cancer (BCa) has not been fully elucidated. Here, we reported that TRIP13 expression was elevated in BCa tissues compared with normal bladder tissues. Notably, the increased expression of TRIP13 was correlated with advanced tumor stage, lymph node metastasis, distant metastasis and reduced survival in BCa patients. Knockdown of TRIP13 in bladder cancer cells suppressed proliferation, induced cell cycle arrest, promoted apoptosis, and impaired cell motility, ultimately inhibiting tumor xenograft growth. Mechanistic investigations revealed that TRIP13 directly bound to epidermal growth factor receptor (EGFR), modulating the EGFR signaling pathway. Furthermore, TRIP13 expression was positively correlated with EGFR expression in BCa specimens, and the high expression of both TRIP13 and EGFR predicted poor survival. Overall, our results underscore the crucial role of TRIP13 in the tumorigenesis of BCa and provide a novel biomarker and therapeutic target for BCa treatment.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据