MiR-200a-3p promotes the proliferation of human esophageal cancer cells by post-transcriptionally regulating cytoplasmic collapsin response mediator protein-1

Abstract

The dysregulation of cytoplasmic collapsin response mediator protein 1 (CRMP1) has been reported in lung cancer, medulloblastoma and esophageal cancer. However, the role of CRMP1 and its regulatory mechanisms in esophageal cancer remain unclear. In this study, we demonstrated that CRMP1 expression was downregulated in esophageal cancer tissues and that there were differences in its expression levels in different esophageal cancer cell lines. We found that CRMP1 overexpression inhibited the proliferation of esophageal cancer cells, whereas the silencing of CRMP1 promoted cell proliferation. We performed an analysis of potential microRNA (miRNA or miR) target sites using a commonly used prediction algorithm (TargetScan). The algorithm predicted that miR200a-3p targets the 3' untranslated region (3'UTR) of CRMP1. Further experiments confirmed this prediction. In addition, we found that miR200a-3p promoted the proliferation of esophageal cancer cells. Thus, our findings indicate that miR200a-3p promotes the proliferation of human esophageal cancer cells by post-transcriptionally regulating CRMP1.