PDZ连接激酶,又一新的原癌基因

PDZ-binding Kinase,a New Proto-oncogene

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DOI 10.16476/j.pibb.2020.0213
刊名
年,卷(期) 2021, 48(02)
作者
作者单位 (1)南华大学药物药理研究所;
2)桂林医学院药学院;
3)桂林医学院第二附属医院

摘要
PDZ连接激酶(PBK)是一种丝-苏氨酸激酶,属于丝裂原活化蛋白激酶激酶(MAPKK)家族成员.PBK能调控细胞周期进程,促进细胞增殖.近年发现,其在乳腺癌、结肠癌、皮肤癌和前列腺癌等多种恶性肿瘤组织中均呈高表达,与多种癌症预后不良关联密.PBK主要通过Wnt、PI3K/AKT/mTOR和MAPK等信号通路,调控肿瘤细胞有丝分裂,参与多种癌症的增殖、侵袭转移和耐药等,并受miR-216b-3p、miR-770-5p和miR-372-5p等多种microRNA调控.提示PBK可能作为又一新的原癌基因,有望成为抑癌药物新的分子靶点.
Abstract
PDZ-binding kinase (PBK), a member of the mitogen-activated protein kinase kinase (MAPKK)family, is a silk-threonine kinase containing 322 amino acids. Its protein is mainly expressed in the tissues withhigh proliferation potential, testis, placenta, activated T cells and neural progenitor cells while extremely low in the tissues and cells with a high degree of differentiation. In recent years, PBK expression has been found significantly enhanced in a variety of malignant tumor such as breast, colon, liver, lung, prostate, esophageal cancer, and so on, closely related to poor prognosis of the cancers mentioned above. Further studies have pointed out that PBK can also promote the proliferation, invasion and metastasis of many cancer cells through a series of complex signaling pathways including Wnt, PI3K/AKT/mTOR, MAPK, FOXM1, nuclear factor-κB and matrix metalloproteinase (MMP), and participate in drug resistance. Moreover, the role of PBK has been confirmed controlled by different microRNA like miR-216b-3p, miR-770-5p and miR-372-5p in the cancers. All above suggest that PBK might be a new proto-oncogene, which is expected to become a new molecular target for tumor suppressor drugs.
关键词
PDZ连接激酶,原癌基因,增殖,侵袭转移,耐药,microRNA调控
KeyWord
PDZ-binding kinase (PBK), proto-oncogene, proliferation, invasion and metastasis, drug resistance,controlled by microRNA
基金项目
页码 184-191
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杨瑞霞, 谢伟全,王文敬,于水灵,周志刚,涂 剑,. PDZ连接激酶,又一新的原癌基因 [J]. 生物化学与生物物理进展. 2021; 48; (02). 184 - 191.

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