Dexmedetomidine represses proliferation and promotes apoptosis of esophageal cancer cells by regulating C-Myc gene expression via the ERK signaling pathway.

Abstract

The aim of this study was to investigate the effects of dexmedetomidine (DEX) on proliferation and apoptosis of esophageal cancer (EC) cells, and to explore the possible underlying mechanism. EC cells (Eca109) were randomly divided into two groups, namely, Control group and DEX group. The viability, proliferation, and apoptosis of Eca109 cells were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, 5-Ethynyl-2'-deoxyuridine (EdU) staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining, respectively. Meanwhile, the messenger ribonucleic acid (mRNA) and protein expression levels of extracellular signal-regulated kinase (ERK) 1/2 and c-Myc in Eca109 cells were measured by quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) and Western blotting, respectively. The viability of Eca109 cells was remarkably weakened in DEX group when compared with Control group (p<0.05). DEX could significantly inhibit the proliferation and promote the apoptosis of Eca109 cells (p<0.05). Moreover, the mRNA and protein levels of ERK1/2 and c-Myc in Eca109 cells declined notably (p<0.05). DEX represses the proliferation and facilitates the apoptosis of Eca109 cells prominently. The possible underlying mechanism may be associated with the inhibition of c-Myc gene expression through the ERK signaling pathway.