Liu Na, Ling Rui, Tang Xiang, Yu Yunpeng, Zhou Yuepeng, Chen Deyu
Institute of Oncology, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Front Oncol. 2022 Mar 21;12:847701. doi: 10.3389/fonc.2022.847701. eCollection 2022.
Bromodomain-containing protein 4 (BRD4), a member of the bromodomain and extraterminal (BET) family, is considered to be a major driver of cancer cell growth and a new target for cancer therapy. Over 30 targeted inhibitors currently in preclinical and clinical trials have significant inhibitory effects on various tumors, including acute myelogenous leukemia (AML), diffuse large B cell lymphoma, prostate cancer, breast cancer and so on. However, resistance frequently occurs, revealing the limitations of BET inhibitor (BETi) therapy and the complexity of the BRD4 expression mechanism and action pathway. Current studies believe that when the internal and external environmental conditions of cells change, tumor cells can directly modify proteins by posttranslational modifications (PTMs) without changing the original DNA sequence to change their functions, and epigenetic modifications can also be activated to form new heritable phenotypes in response to various environmental stresses. In fact, research is constantly being supplemented with regards to that the regulatory role of BRD4 in tumors is closely related to PTMs. At present, the PTMs of BRD4 mainly include ubiquitination and phosphorylation; the former mainly regulates the stability of the BRD4 protein and mediates BETi resistance, while the latter is related to the biological functions of BRD4, such as transcriptional regulation, cofactor recruitment, chromatin binding and so on. At the same time, other PTMs, such as hydroxylation, acetylation and methylation, also play various roles in BRD4 regulation. The diversity, complexity and reversibility of posttranslational modifications affect the structure, stability and biological function of the BRD4 protein and participate in the occurrence and development of tumors by regulating the expression of tumor-related genes and even become the core and undeniable mechanism. Therefore, targeting BRD4-related modification sites or enzymes may be an effective strategy for cancer prevention and treatment. This review summarizes the role of different BRD4 modification types, elucidates the pathogenesis in the corresponding cancers, provides a theoretical reference for identifying new targets and effective combination therapy strategies, and discusses the opportunities, barriers, and limitations of PTM-based therapies for future cancer treatment.
含溴结构域蛋白4(BRD4)是溴结构域与额外末端(BET)家族的成员之一,被认为是癌细胞生长的主要驱动因素及癌症治疗的新靶点。目前超过30种处于临床前和临床试验阶段的靶向抑制剂对包括急性髓系白血病(AML)、弥漫性大B细胞淋巴瘤、前列腺癌、乳腺癌等在内的多种肿瘤具有显著抑制作用。然而,耐药性频繁出现,揭示了BET抑制剂(BETi)治疗的局限性以及BRD4表达机制和作用途径的复杂性。目前的研究认为,当细胞的内外环境条件发生变化时,肿瘤细胞可通过翻译后修饰(PTM)直接修饰蛋白质而不改变原始DNA序列来改变其功能,并且表观遗传修饰也可被激活以响应各种环境应激形成新的可遗传表型。事实上,关于BRD4在肿瘤中的调节作用与PTM密切相关的研究正在不断补充。目前,BRD4的PTM主要包括泛素化和磷酸化;前者主要调节BRD4蛋白的稳定性并介导BETi耐药,而后者与BRD4的生物学功能相关,如转录调控、辅因子募集、染色质结合等。同时,其他PTM,如羟基化、乙酰化和甲基化,在BRD4调节中也发挥着各种作用。翻译后修饰的多样性、复杂性和可逆性影响BRD4蛋白的结构、稳定性和生物学功能,并通过调节肿瘤相关基因的表达参与肿瘤的发生发展,甚至成为核心且不可忽视的机制。因此,靶向BRD4相关修饰位点或酶可能是癌症防治的有效策略。本综述总结了不同BRD4修饰类型的作用,阐明了在相应癌症中的发病机制,为识别新靶点和有效的联合治疗策略提供理论参考,并讨论了基于PTM的疗法在未来癌症治疗中的机遇、障碍和局限性。