Upregulation of long non-coding RNA CCAT1 promotes proliferation and metastasis of esophageal squamous cell carcinoma cells by regulating the miR-543/KRAS axis

Abstract

Dysregulation of long non-coding RNA (lncRNAs) plays vital roles in tumorigenesis and cancer progression. Previous studies have identified the role of the lncRNA CCAT1 as an oncogene in several cancer types, and ectopic expression of CCAT1 predicts a poor prognosis. This study sought to determine the underlying mechanism for this observation in esophageal squamous cell carcinoma (ESCC). We found that CCAT1 was significantly upregulated in human ESCC tumor tissues and cell lines. LncRNA CCAT1 overexpression enhanced cell proliferation, migration, and invasion in vitro and in vivo. Our bioinformatics analysis and RNA immunoprecipitation assays combined with dual-luciferase assays revealed that CCAT1 functions as a microRNA (miRNA) sponge for miR-543. Increased CCAT1 antagonized the functions of miRNA-543 and led to de-repression of its downstream target, KRAS, which is a core oncogene that facilitates ESCC progression. Our findings suggest that CCAT1 increases KRAS expression by sponging miR-543 and thus promotes ESCC progression. This study sheds light on the potential role of lncRNAs as a novel prognostic biomarker and provides a new therapeutic target for ESCC.