Abstract
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].
Highlights
Data on the association of CMPK1 with clinicopathological features and biological effect in human epithelial ovarian cancer
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 transforming growth factor-β (TGF-β) signalling pathway through the upregulation of miR-130b-3p in human epithelial ovarian cancer” [1]
CMPK is an enzyme required for nucleic acid biosynthesis [4] and is regulated by the TGF-β signaling pathway in EOC cells [1]
Summary
Data on the association of CMPK1 with clinicopathological features and biological effect in human epithelial ovarian cancer. 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].
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