Objective: To investigate the effect of simvastatin (hydrophobic statin) andpravastatin (hydrophilic statin) on the cell proliferation of esophagealadenocarcinoma (EAC)/esophageal squamous cell carcinoma (ESCC) and therelated expression of cyclooxygenase-2(COX-2) pathway productions, and toexplore the potential anti-cancer effects and probable mechanisms of statins onesophageal cancer.Methods: Eca-109(ESCC) or OE-19(EAC) cells were treated with6differentconcentrations, including15,30,45,60and75μM of simvastatin or pravastatin for24and48h, respectively. Culture medium and0.1%DMSO (for simvastatin only)were used for blank control and salute control groups. Cell proliferation wasassessed by Cell Counting Kit-8assay. The concentrations of MDA were measuredby Thiobarbituric acid (TBA) method. Messenger RNA (mRNA) and proteinexpression of COX-2were determined by reverse transcriptase-polymerase chainreaction (RT-PCR) and Western blot, respectively. The expression of prostaglandinE2(PGE2) was measured by ELISA.Results: Cell growth of both Eca-109and OE-19cells treated by simvastatin wereinhibited in a concentration-dependent manner, which were companied by theinhibition of COX-2mRNA, protein expression and down-regulation of PGE2expression. However, significant differences were found only in the higherconcentration groups (30μM and beyond)(p<0.05). No effect on the cellproliferation of EAC or ESCC was found in pravastatin treated cells (p>0.05).Up-regulation of MDA were found in simvastatin treated Eca-109cells and OE-19cells in a concentration-dependent manner (p<0.05), while no alteration of that was found in the pravastatin-treated groups.(p>0.05).Conclusions: Simvastatin inhibited the cell growth of both Eca-109and OE-19cells,which may result in the inhibiton of COX-2and PGE2expression. Pravastatinshowed no effect on the cell proliferation of EAC or ESCC cells in vitro. |