Laboratório de Biologia Celular, Departamento de Ciências Básicas da Saúde, Universidade Federal de Ciências da Saúde de Porto Alegre (UFCSPA), Rua Sarmento Leite, Rua Sarmento Leite, No. 245, 90050-170 Porto Alegre, RS, Brazil.
Biomed Res Int. 2014;2014:123010. doi: 10.1155/2014/123010. Epub 2014 Jun 23.
The protooncogene PCPH was recently identified as being the ectonucleoside triphosphate diphosphohydrolase 5 (ENTPD5). This protooncogene is converted into an oncogene by a single base pair deletion, resulting in frame change and producing a premature stop codon, leading to a mutated protein (mt-PCPH) with only 27 kDa, which is much smaller than the original 47 kDa protein. Overexpression of the PCPH as well as the mutated PCPH increases the cellular resistance to stress and apoptosis. This is intriguing considering that the active form, that is, the oncogene, is the mutated PCPH. Several studies analyzed the expression of NTPDase5/mt-PCPH in a wide range of tumor cells and evaluated its role and mechanisms in cancer and other pathogenic processes. The main point of this review is to integrate the findings and proposed theories about the role played by NTPDase5/mt-PCPH in cancer progression, considering that these proteins have been suggested as potential early diagnostic tools and therapy targets.
原癌基因 PCPH 最近被确定为外核苷酸三磷酸二磷酸水解酶 5（ENTPD5）。该原癌基因通过单个碱基对缺失转化为癌基因，导致框架改变并产生过早的终止密码子，导致仅具有 27 kDa 的突变蛋白（mt-PCPH），远小于原始的 47 kDa 蛋白。PCPH 的过表达以及突变的 PCPH 增加了细胞对应激和细胞凋亡的抵抗力。这令人感到好奇，因为活性形式，即癌基因，是突变的 PCPH。几项研究分析了 NTPDase5/mt-PCPH 在广泛的肿瘤细胞中的表达，并评估了其在癌症和其他致病过程中的作用和机制。本篇综述的主要观点是整合关于 NTPDase5/mt-PCPH 在癌症进展中所起作用的研究结果和提出的理论，因为这些蛋白被认为是潜在的早期诊断工具和治疗靶标。
