CERS6 antisense RNA 1 promotes colon cancer via upregulating mitochondrial calcium uniporter

Abstract

AbstractBackgroundColon cancer (CC) belongs to a common cancer of digestive system. Long non‐coding RNAs (lncRNAs) are dysregulated in numerous cancers and affect their development. The function of lncRNA CERS6 antisense RNA 1 (CERS6‐AS1) in CC remains unclear.Materials and MethodsCERS6‐AS1 expression in colon adenocarcinoma tissues and CC cell lines was assessed by The Cancer Genome Atlas database and quantitative real‐time polymerase chain reaction analysis. The function of CERS6‐AS1 in CC was analysed by 5‐ethynyl‐2′‐deoxyuridine, colony formation, flow cytometry, terminal deoxynucleotidyl transferase dUTP nick end labelling, wound healing, Transwell and immunofluorescence assays. Mechanistic analyses including RNA pull down, RNA‐binding protein immunoprecipitation and luciferase reporter assay revealed the interaction between RNAs.ResultsCERS6‐AS1 expression was aberrantly upregulated in colon adenocarcinoma tissues and CC cell lines. CERS6‐AS1 knockdown inhibited CC cell malignant phenotypes and in vivo tumour growth. CERS6‐AS1 served as the competing endogenous RNA of microRNA‐16‐5p in CC, and microRNA‐16‐5p inhibition partly rescued the effects of CERS6‐AS1 depletion on CC development. Mitochondrial calcium uniporter was targeted by microRNA‐16‐5p. Mitochondrial calcium uniporter upregulation completely remedied the influence of CERS6‐AS1 silencing in CC progression. Moreover, CERS6‐AS1 enhanced the stability of mitochondrial calcium uniporter messenger RNA via recruiting RNA‐binding protein embryonic lethal abnormal vision like 1.ConclusionCERS6‐AS1 promotes the development of CC via upregulating mitochondrial calcium uniporter expression.