Abstract
Background and objectiveLong-term statin therapy has been shown to protect against several cancers, including esophageal cancer (EC). While the mechanisms underlying this effect are not clear. We investigated the effect of hydrophobic simvastatin and hydrophilic pravastatin on the proliferation of EC cells and sought to explore the underlying mechanisms.MethodsEsophageal adenocarcinoma OE-19 cells and esophageal squamous cell carcinoma Eca-109 cells were treated with different concentrations of simvastatin or pravastatin for 24 h and 48 h. Cell proliferation was assessed by Cell Counting Kit-8 assay. Malondialdehyde (MDA) levels were measured by thiobarbituric acid (TBA) assay. mRNA and protein expression of COX-2 were determined by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot, respectively; The expression of prostaglandin E2 (PGE2) was measured by ELISA.ResultsSimvastatin, but not pravastatin, significantly inhibited the proliferation of OE-19 and Eca-109 cells in a dose- and time-dependent manner, accompanying with the increasing of the MDA level. Moreover, simvastatin suppressed the expression of COX-2 and PGE2 in both OE-19 and Eca-109 cells in a dose-dependent manner.ConclusionsLipophilic simvastatin, but not hydrophilic pravastatin, had significant inhibitory effects on the proliferation of Eca-109 and OE-19 cells. The reduction of COX-2 and PGE2 by simvastatin suggested that the inhibitory effect of simvastatin on the proliferation of EC cells may be independent of its lipid-lowering effect. Simvastatin may be a promising agent for the prevention and treatment of EC.
Highlights
Background and objectiveLong-term statin therapy has been shown to protect against several cancers, including esophageal cancer (EC)
We investigated the effect of lipophilic simvastatin and hydrophilic pravastatin on the proliferation of esophageal cancer adenocarcinoma OE-19 cells and esophageal squamous cell carcinoma Eca-109 cells, and analyzed their effect on the expression of COX-2 and its downstream product prostaglandin E2 (PGE2)
Simvastatin, but not pravastatin, inhibited the proliferation of EC cells Both OE-19 and Eca-109 cell proliferation was blunted by simvastatin in a dose- and time- dependant manner, with statin concentrations of 30 μM and above producing statistically significant reductions (Fig. 1a)
Summary
Background and objectiveLong-term statin therapy has been shown to protect against several cancers, including esophageal cancer (EC). While the mechanisms underlying this effect are not clear. We investigated the effect of hydrophobic simvastatin and hydrophilic pravastatin on the proliferation of EC cells and sought to explore the underlying mechanisms. Esophageal adenocarcinoma (EAC) and esophageal squamous cell carcinoma (ESCC) are two different pathological types of esophageal cancer (EC). The worldwide incidence of both EAC and ESCC are still high, there is a lack of effective agents for the prevention and treatment of EC. In a case-control study [7], statins were shown to reducing the risk of EAC by 48%, but there is no study investigating the role of statins in the prevention of ESCC. Since ESCC is the dominant type of EC in China, it should be interesting to study the effects of statins on the prevention of ESCC
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