肝再生磷酸酶2的促癌机制及其抑制剂的研究进展
The oncogenic mechanism of phosphatase of regenerating liver 2 and the research progress of its inhibitors
李茹薇 1陶浩强 2肖奕菲 1王佳银 1于洁2
作者信息
- 1. 杭州医学院存济口腔医学院,杭州 310013
- 2. 杭州医学院检验医学院、生物工程学院,浙江省神经精神疾病药物研究重点实验室,杭州 310013
- 折叠
摘要
肝再生磷酸酶2(phosphatase of regenerating liver 2,PRL2)属于肝再生磷酸酶家族,在人体各个组织器官中广泛表达.PRL2异常高表达与肿瘤的发生发展和临床预后密切相关,是多种癌症的潜在治疗靶点.研究表明PRL2通过两种机制发挥促癌作用:一是依赖假磷酸酶活性,主要与镁离子转运体CNNM3结合;二是凭借磷酸酶活性,使底物分子PTEN等去磷酸化.因此,阻断PRL2与CNNM3结合或抑制PRL2磷酸酶活性有望成为新的抗癌策略.现综述了 PRL2与不同癌症的联系、其促癌分子机制和抑制剂的最新研究进展.
Abstract
The phosphatase of regenerating liver 2(PRL2),a member of the phosphatases of regenerating liver,exhibits widespread expression throughout various tissues and organs in the human body.Elevated expression of PRL2 is closely associated with the initiation,progression,and clinical outcomes of tumors,rendering it a prospective therapeutic target across various malignancies.Studies indicate that PRL2 functions in cancer progression through two mechanisms:firstly,it leverages pseudophosphatase activity,which mainly interacts with the magnesium ion transporter CNNM3;the second is to utilize phosphatase activity to dephosphorylate substrate molecules such as PTEN.Consequently,strategies aimed at disrupting the interaction between PRL2 and CNNM3 or inhibting the phosphatase activity of PRL2 represent novel avenues for anticancer intervention.This review comprehensively outlines the associations between PRL2 with diverse cancers,elucidating the molecular mechanisms underlying its oncogenic properties and the latest advancements of its inhibitors.
关键词
肝再生磷酸酶2/癌症/细胞周期蛋白M3/磷酸酶及张力蛋白同源物/抑制剂Key words
phosphatase of regenerating liver 2/cancer/cyclin-M3/phosphatase and tensin homolog/inhibitor引用本文复制引用
基金项目
浙江省自然科学基金项目(LQ21H310006)
浙江省医药卫生科技计划项目(2024KY921)
浙江省教育厅高校一般科研项目(Y202352851)
国家级大学生创新创业训练计划项目(202313023012)
出版年
2024
NETL
NSTL
万方数据