中心体
生物
有丝分裂
癌症
细胞周期
核分裂突变
癌症研究
癌细胞
细胞生长
细胞生物学
遗传学
作者
Özge Saatci,Özgür Şahin
出处
期刊:Cell Cycle
[Informa]
日期:2023-12-17
卷期号:22 (23-24): 2637-2655
被引量:1
标识
DOI:10.1080/15384101.2024.2302243
摘要
TACC3 is the most oncogenic member of the transforming acidic coiled-coil domain-containing protein (TACC) family. It is one of the major recruitment factors of distinct multi-protein complexes. TACC3 is localized to spindles, centrosomes, and nucleus, and regulates key oncogenic processes, including cell proliferation, migration, invasion, and stemness. Recently, TACC3 inhibition has been identified as a vulnerability in highly aggressive cancers, such as cancers with centrosome amplification (CA). TACC3 has spatiotemporal functions throughout the cell cycle; therefore, targeting TACC3 causes cell death in mitosis and interphase in cancer cells with CA. In the clinics, TACC3 is highly expressed and associated with worse survival in multiple cancers. Furthermore, TACC3 is a part of one of the most common fusions of FGFR, FGFR3-TACC3 and is important for the oncogenicity of the fusion. A detailed understanding of the regulation of TACC3 expression, its key partners, and molecular functions in cancer cells is vital for uncovering the most vulnerable tumors and maximizing the therapeutic potential of targeting this highly oncogenic protein. In this review, we summarize the established and emerging interactors and spatiotemporal functions of TACC3 in cancer cells, discuss the potential of TACC3 as a biomarker in cancer, and therapeutic potential of its inhibition.
科研通智能强力驱动
Strongly Powered by AbleSci AI