Zhang Chuanyong, Ni Chuangye, Lu Hao
Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China.
Front Oncol. 2022 Jul 8;12:956225. doi: 10.3389/fonc.2022.956225. eCollection 2022.
Polo-like kinase (PLK) 2 is an evolutionarily conserved serine/threonine kinase that shares the n-terminal kinase catalytic domain and the C-terminal Polo Box Domain (PBD) with other members of the PLKs family. In the last two decades, mounting studies have focused on this and tried to clarify its role in many aspects. PLK2 is essential for mitotic centriole replication and meiotic chromatin pairing, synapsis, and crossing-over in the cell cycle; Loss of PLK2 function results in cell cycle disorders and developmental retardation. PLK2 is also involved in regulating cell differentiation and maintaining neural homeostasis. In the process of various stimuli-induced stress, including oxidative and endoplasmic reticulum, PLK2 may promote survival or apoptosis depending on the intensity of stimulation and the degree of cell damage. However, the role of PLK2 in immunity to viral infection has been studied far less than that of other family members. Because PLK2 is extensively and deeply involved in normal physiological functions and pathophysiological mechanisms of cells, its role in diseases is increasingly being paid attention to. The effect of PLK2 in inhibiting hematological tumors and fibrotic diseases, as well as participating in neurodegenerative diseases, has been gradually recognized. However, the research results in solid organ tumors show contradictory results. In addition, preliminary studies using PLK2 as a disease predictor and therapeutic target have yielded some exciting and promising results. More research will help people better understand PLK2 from principle to practice.
Polo样激酶(PLK)2是一种进化上保守的丝氨酸/苏氨酸激酶,与PLKs家族的其他成员共享N端激酶催化结构域和C端Polo盒结构域(PBD)。在过去二十年中,越来越多的研究聚焦于此,并试图阐明其在许多方面的作用。PLK2对有丝分裂中心粒复制以及细胞周期中的减数分裂染色质配对、联会和交叉至关重要;PLK2功能丧失会导致细胞周期紊乱和发育迟缓。PLK2还参与调节细胞分化和维持神经稳态。在包括氧化应激和内质网应激等各种刺激诱导的应激过程中,PLK2可能根据刺激强度和细胞损伤程度促进细胞存活或凋亡。然而,PLK2在病毒感染免疫中的作用研究远少于其他家族成员。由于PLK2广泛且深入地参与细胞的正常生理功能和病理生理机制,其在疾病中的作用越来越受到关注。PLK2在抑制血液系统肿瘤和纤维化疾病以及参与神经退行性疾病方面的作用已逐渐得到认可。然而,实体器官肿瘤的研究结果却相互矛盾。此外,将PLK2用作疾病预测指标和治疗靶点的初步研究已经取得了一些令人兴奋且有前景的结果。更多的研究将有助于人们从原理到实践更好地理解PLK2。