Tumor-Promoting ATAD2 and Its Preclinical Challenges.
Tumor-Promoting ATAD2 and Its Preclinical Challenges.
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促肿瘤 ATAD2 及其临床前挑战。
DOI：
10.3390/biom12081040
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发表时间：
2022-07-28
期刊：
影响因子：
5.5
通讯作者：
中科院分区：
文献类型：
--
作者：
ATAD 2作为一种在多种恶性肿瘤中具有促癌作用的潜在癌基因，近年来受到广泛关注。ATAD 2是一个高度保守的布罗莫结构域家族蛋白，主要通过AAA ATP酶和布罗莫结构域发挥其生物学功能。ATAD 2作为表观遗传解码器和转录因子或共激活因子，参与细胞活动，如转录调控、DNA复制和蛋白质修饰。据报道，ATAD 2在多种人类恶性肿瘤中高度表达，包括胃肠道恶性肿瘤、生殖系统恶性肿瘤、泌尿系统恶性肿瘤、肺癌和其他类型的恶性肿瘤。ATAD 2参与多种致癌信号通路的激活，与肿瘤的发生、进展、化疗耐药性和预后不良密切相关，但不同类型癌症的致癌机制不同。此外，直接靶向ATAD 2的布罗莫结构域可能是一项非常具有挑战性的任务。本文就ATAD 2在各种恶性肿瘤中的作用进行综述，并指出其药理学研究方向。
ATAD2 has received extensive attention in recent years as one prospective oncogene with tumor-promoting features in many malignancies. ATAD2 is a highly conserved bromodomain family protein that exerts its biological functions by mainly AAA ATPase and bromodomain. ATAD2 acts as an epigenetic decoder and transcription factor or co-activator, which is engaged in cellular activities, such as transcriptional regulation, DNA replication, and protein modification. ATAD2 has been reported to be highly expressed in a variety of human malignancies, including gastrointestinal malignancies, reproductive malignancies, urological malignancies, lung cancer, and other types of malignancies. ATAD2 is involved in the activation of multiple oncogenic signaling pathways and is closely associated with tumorigenesis, progression, chemoresistance, and poor prognosis, but the oncogenic mechanisms vary in different cancer types. Moreover, the direct targeting of ATAD2’s bromodomain may be a very challenging task. In this review, we summarized the role of ATAD2 in various types of malignancies and pointed out the pharmacological direction.
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影响因子：
5.8
作者：
Yang J;Huang J;Luo L;Chen Z;Guo Y;Guo L
通讯作者：
Guo L
影响因子：
--
作者：
Altintas, D. M.;Shukla, M. S.;Samarut, Jacques
通讯作者：
Samarut, Jacques
影响因子：
4.2
作者：
Duan, Zhijian;Andrews, Nicolas P.;Chen, Hong-Wu
通讯作者：
Chen, Hong-Wu
DOI：
10.1002/anie.201603928
发表时间：
2016-09-12
期刊：
Angewandte Chemie (International ed. in English)
影响因子：
--
作者：
Bamborough P;Chung CW;Demont EH;Furze RC;Bannister AJ;Che KH;Diallo H;Douault C;Grandi P;Kouzarides T;Michon AM;Mitchell DJ;Prinjha RK;Rau C;Robson S;Sheppard RJ;Upton R;Watson RJ
通讯作者：
Watson RJ
影响因子：
2.1
作者：
Chen, Dong;Maruschke, Matthias;Buchner, Alexander
通讯作者：
Buchner, Alexander