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

机译:CMPK1与人上皮性卵巢癌的临床病理特征和生物学效应的关系数据

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摘要

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” . CMPK, as well as cystatin B and β-2-microglobulin , is overexpressed in human epithelial-type ovarian tumors. CMPK is an enzyme required for nucleic acid biosynthesis and is regulated by the TGF-β signaling pathway in EOC cells . 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 .
机译:人上皮性卵巢癌(EOC)是最致命的妇科疾病。但是,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。本数据显示胞苷单磷酸激酶(CMPK)作为EOC生物标志物,并且与题为“胞苷单磷酸激酶通过上调卵巢上皮性卵巢癌中的miR-130b-3p的表达而被TGF-β信号通路抑制”有关。 CMPK以及胱抑素B和β-2-微球蛋白在人上皮型卵巢肿瘤中过表达。 CMPK是核酸生物合成所需的酶,并受EOC细胞中TGF-β信号通路的调节。此外,数据显示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的调控,其中一些miRNA可能影响EOC的化学抗性。

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