ObjectiveTo explore the regulatory mechanism of inducible nitric oxide synthase (NOS-2) expression related to proliferation of Tca8113 cells.MethodsRNAi mediated by short hairpin RNAs was utilized to knock down NOS-2, protein kinase C (PKC)-α, PKC-β and PKC-δ. Griess Reagent played a significant role on the detection of NO product after NOS-2 silence. The cell proliferation was determined by CCK8 method. Quantitative real-time polymerase chain reaction (q-PCR) was recruited to check the mRNA level of NOS-2, PKC-α, PKC-β and PKC-δ after treated by a variety of ways. Eventually, the measure of phosphorylation of extracellular regulated protein kinases (ERK)1/2 was performed by Western blotting in PMA-treated Tca8113 cells.ResultsThe cell viability of Tca8113 decreased obviously after transfected with NOS-2 siRNA (P<0 .01). pkc reduced the expression level of nos-2 mrna (P<0 .05). pkc-α, pkc-β and pkc-δ worked together to regulate the level of nos-2 mrna (P<0 .01). motigen-activated protein kinase kinase (mek)/erk signaling pathway regulated the level of nos-2 mrna negatively (P<0 .05). pkc down regulated the level of nos-2 mrna through mek/erk signaling pathway (P<0 .05).ConclusionPKC regulates the mRNA level of NOS-2 related to proliferation through MEK/ERK signaling pathway in Tca8113 cells..
