Long Non-Coding RNA Reprogramming (ROR) Promotes Cell Proliferation in Colorectal Cancer via Affecting P53.

Abstract

BackgroundColorectal cancer (CRC) remains one of the most common lethal malignant tumors worldwide. The correlation between lncRNAs expression and CRC development has not been well identified in the recent literature. This study focused on the role of lncRNA-ROR on CRC progression and development.Material/MethodsQuantitative real-time PCR (qRT-PCR) assay was conducted to identify the expression level of lncRNA-ROR. Cell proliferation and viability were examined by MTT assay and colony formation assay. Cell cycle distribution and apoptosis were detected by flow cytometry. Expressions of p53, p21, and FAS protein levels were assessed by Western blotting. CRC cells transfected with lncRNA-shRNA were injection into nude mice to identify the function of lncRNA-ROR on tumorigenesis in vivo.ResultsThe expression level of lncRNA-ROR was elevated in CRC tissues when compared to adjacent tissues (n=78). lncRNA-ROR knockdown significantly suppressed cell proliferation and viability, while lncRNA-ROR overexpression had the opposite effect. Decreased lncRNA-ROR expression enhanced cell apoptosis and triggered cell cycle arrest in G0/G1 phase, while elevated lncRNA-ROR expression presented the opposite effect. Protein levels of p53 and p53 target genes were affected by lncRNA-ROR in vitro, and downregulation of lncRNA-ROR impeded tumorigenesis in vivo.ConclusionsOur study demonstrates that lncRNA-ROR participates in controlling CRC proliferation, viability, and apoptosis, partially by modulating p53, which provides potential and prospective therapeutic targets for CRC.