Ren Xin, Shan Wen-Hua, Wei Lu-Lu, Gong Chan-Chan, Pei Dong-Sheng
Jiangsu Key Laboratory of Biological Cancer Therapy Xuzhou Medical University, Xuzhou 221002, China.
Department of Oncology, The Jiangyin Clinical College of Xuzhou Medical University, Jiangyin, Jiangsu 214400, China.
Anticancer Agents Med Chem. 2018;18(8):1082-1090. doi: 10.2174/1871520618666180411123447.
Tartrate-resistant acid phosphatase 5 (ACP5) is an evolutionarily conserved and multifunctional protein that is involved in generations of reactive oxygen species, normal bone development, osteoblast regulation and macrophage function, affecting a series of pathways, as well as reflecting bone resorption and osteoclast activity.
Literature searches, systematic reviews and assessments about the structure, distribution, regulation and novel functions of ACP5 were performed in this review from PubMed and Medline databases.
Studies demonstrate that RANKL can increase the expression of ACP5 through NFATc1 and c-Fos to accelerate osteoclastogenesis, which also can be regulated by many regulators. Based on the aforementioned information, it is shown that ACP5, together with the phosphatase activity, can medicate the progression and development of human genetic diseases and cancer.
As a novel target, ACP5 plays a critical role in preventing, monitoring and treating various kinds of tumors, as well as accelerating the development of a promising therapeutic strategy for human genetic diseases. However, the explicit mechanism between ACP5 and cancer is not so clear. It is necessary and significant for us to pay more in-depth attention.
抗酒石酸酸性磷酸酶5（ACP5）是一种进化保守的多功能蛋白质，参与活性氧的产生、正常骨骼发育、成骨细胞调节和巨噬细胞功能，影响一系列信号通路，同时反映骨吸收和破骨细胞活性。
本综述通过检索PubMed和Medline数据库，对ACP5的结构、分布、调节及新功能进行文献检索、系统评价和分析。
研究表明，核因子κB受体活化因子配体（RANKL）可通过活化T细胞核因子c1（NFATc1）和原癌基因c-Fos增加ACP5的表达，从而加速破骨细胞生成，且其表达受多种调节因子调控。基于上述信息，研究显示ACP5及其磷酸酶活性可介导人类遗传病和癌症的进展与发展。
作为一个新的靶点，ACP5在预防、监测和治疗各类肿瘤以及加速人类遗传病治疗策略的开发中发挥着关键作用。然而，ACP5与癌症之间的确切机制尚不清楚，有必要进行更深入的研究。
