Those deoxycytidine analogs have to be phosphorylated stepwise to their triphosphate forms before they can be incorporated into cellular or viral DNA and/or RNA for anticancer and antiviral effects. UMP/CMP kinase activity should be pivotal for the cytotoxic effect of cytidine analogs in Procaterol hydrochloride target cells because it is responsible for the phosphorylation of these cytidine analog monophosphates or 5-FU monophosphate to their diphosphate metabolites in anticancer and antiviral therapy. Gemcitabine and troxacitabine are anticancer PHA-543613 agents that are currently being used or under clinical trials for the treatment of cancer. Although the configurations of dFdC and L-OddC are different, the first two steps in their metabolism appear to be the same. Both dFdC and L-OddC are phosphorylated by the cytoplasmic deoxycytidine kinase to their respective monophosphate metabolites, and the so-called UMP/CMP kinase in vitro can phosphorylate dFdC and L-OddC monophosphates to their diphosphate metabolites. Their in vitro Km values are 450�C 581 mM with Vmax 3.6�C31 mmol/mg/min and 1037 mM with Vmax 0.63 mmol/mg/min, respectively. There are many enzymes involved in 5-FU metabolism, in which this UMP/CMP kinase was thought to play an important role in the activation of 5-FU to 5FUTP/5FdUTP and its incorporation into RNA and DNA. Although the UMP/CMP kinase is suggested to be the enzyme responsible for the phosphorylation of CMP and UMP as well as some cytidine analog monophosphates, there is little information in cells to support the current dogma. The current knowledge indicated that the KEGG metabolic pathway database has represented a network of interacting molecules as well as compensatory and regulatory pathways during pyrimidine metabolism in cells. However, a gene is not functionally identified until its phosphorylation target is identified or until the role on the biochemical pathway is identified. MicroRNAs are short, endogenous, single-stranded RNA molecules that regulate gene expression by promoting RNA transcript degradation or translation inhibition of target mRNAs. MiRNA genes are transcribed in most cases by RNA polymerase II into primary miRNA transcripts.