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尿苷-胞苷激酶样-1 核苷激酶活性的特征及其在肿瘤生长中的作用。

Characterization of uridine-cytidine kinase like-1 nucleoside kinase activity and its role in tumor growth.

机构信息

Department of Pathology, Saint Louis University School of Medicine, St. Louis, MO, U.S.A.

VA St. Louis Health Care System, St. Louis, MO, U.S.A.

出版信息

Biochem J. 2022 Jun 17;479(11):1149-1164. doi: 10.1042/BCJ20210770.

Abstract

Uridine-cytidine kinase like-1 (UCKL-1) is a largely uncharacterized protein with high sequence similarity to other uridine-cytidine kinases (UCKs). UCKs play an important role in the pyrimidine salvage pathway, catalyzing the phosphorylation of uridine and cytidine to UMP and CMP, respectively. Only two human UCKs have been identified, UCK1 and UCK2. Previous studies have shown both enzymes phosphorylate uridine and cytidine using ATP as the phosphate donor. No studies have evaluated the kinase potential of UCKL-1. We cloned and purified UCKL-1 and found that it successfully phosphorylated uridine and cytidine using ATP as the phosphate donor. The catalytic efficiency (calculated as kcat/KM) was 1.2 × 104 s-1, M-1 for uridine and 0.7 × 104 s-1, M-1 for cytidine. Our lab has previously shown that UCKL-1 is up-regulated in tumor cells, providing protection against natural killer (NK) cell killing activity. We utilized small interfering RNA (siRNA) to down-regulate UCKL-1 in vitro and in vivo to determine the effect of UCKL-1 on tumor growth and metastasis. The down-regulation of UCKL-1 in YAC-1 lymphoma cells in vitro resulted in decreased cell counts and increased apoptotic activity. Down-regulation of UCKL-1 in K562 leukemia cells in vivo led to decreased primary tumor growth and less tumor cell dissemination and metastasis. These results identify UCKL-1 as a bona fide pyrimidine kinase with the therapeutic potential to be a target for tumor growth inhibition and for diminishing or preventing metastasis.

摘要

尿苷-胞苷激酶样-1(UCKL-1)是一种尚未被充分研究的蛋白质,与其他尿苷-胞苷激酶(UCKs)具有高度的序列相似性。UCKs 在嘧啶补救途径中发挥重要作用,分别催化尿苷和胞苷磷酸化为 UMP 和 CMP。目前已鉴定出两种人类 UCK,即 UCK1 和 UCK2。先前的研究表明,两种酶均使用 ATP 作为磷酸供体磷酸化尿苷和胞苷。尚未有研究评估 UCKL-1 的激酶潜能。我们克隆并纯化了 UCKL-1,发现它可成功地使用 ATP 作为磷酸供体磷酸化尿苷和胞苷。其催化效率(以 kcat/KM 计算)分别为 1.2×104 s-1, M-1(对于尿苷)和 0.7×104 s-1, M-1(对于胞苷)。我们实验室先前的研究表明,UCKL-1 在肿瘤细胞中上调,为自然杀伤(NK)细胞杀伤活性提供保护。我们利用小干扰 RNA(siRNA)在体外和体内下调 UCKL-1,以确定 UCKL-1 对肿瘤生长和转移的影响。体外下调 YAC-1 淋巴瘤细胞中的 UCKL-1 导致细胞计数减少和凋亡活性增加。体内下调 K562 白血病细胞中的 UCKL-1 导致原发性肿瘤生长减少,肿瘤细胞扩散和转移减少。这些结果表明 UCKL-1 是一种真正的嘧啶激酶,具有作为肿瘤生长抑制和减少或预防转移的治疗靶标的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0297/9246348/8ed9c3f4adce/BCJ-479-1149-g0001.jpg

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