CMPK1与人类上皮性卵巢癌临床病理特征及生物学效应相关性的数据。

Data on the association of CMPK1 with clinicopathological features and biological effect in human epithelial ovarian cancer.

作者信息

Zhou Daibing, Zhang Lingyun, Lin Qunbo, Ren Weimin, Xu Guoxiong

机构信息

Center Laboratory, Jinshan Hospital, Fudan University, Shanghai 201508, China.

Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.

出版信息

Data Brief. 2017 May 12;13:77-84. doi: 10.1016/j.dib.2017.05.022. eCollection 2017 Aug.

Human epithelial ovarian cancer (EOC) is the most lethal gynecological disease. However, the molecular mechanisms by which transforming growth factor-β (TGF-β) regulates ovarian tumor progression markers remain unclear. The present data show cytidine monophosphate kinase (CMPK) as an EOC biomarker and are related to the article entitled "Cytidine monophosphate kinase is inhibited by the TGF-β signalling pathway through the upregulation of miR-130b-3p in human epithelial ovarian cancer" [1]. CMPK, as well as cystatin B [2] and β-2-microglobulin [3], is overexpressed in human epithelial-type ovarian tumors. CMPK is an enzyme required for nucleic acid biosynthesis [4] and is regulated by the TGF-β signaling pathway in EOC cells [1]. Furthermore, the data show the effect of CMPK-shRNA on EOC cell apoptosis and TGF-β-induced Smad2 phosphorylation. CMPK expression in two EOC cell lines OVCAR-3 and SK-OV-3 is regulated by multiple miRNAs and some of these miRNAs may affect EOC chemoresistance [5].

人上皮性卵巢癌（EOC）是最致命的妇科疾病。然而，转化生长因子-β（TGF-β）调节卵巢肿瘤进展标志物的分子机制仍不清楚。目前的数据表明胞苷单磷酸激酶（CMPK）是一种EOC生物标志物，并且与题为“在人上皮性卵巢癌中，TGF-β信号通路通过上调miR-130b-3p抑制胞苷单磷酸激酶”的文章相关[1]。CMPK以及胱抑素B[2]和β2微球蛋白[3]在人上皮型卵巢肿瘤中过表达。CMPK是核酸生物合成所需的一种酶[4]，并且在EOC细胞中受TGF-β信号通路调节[1]。此外，数据显示了CMPK-shRNA对EOC细胞凋亡和TGF-β诱导的Smad2磷酸化的影响。两种EOC细胞系OVCAR-3和SK-OV-3中的CMPK表达受多种miRNA调节，其中一些miRNA可能影响EOC的化疗耐药性[5]。