LncRNA <i>SNHG16</i> promotes colorectal cancer proliferation by regulating ABCB1 expression through sponging miR-214-3p

Abstract

Mounting evidence indicates that long non-coding RNAs (lncRNAs) have critical roles in colorectal cancer (CRC) progression, providing many potential diagnostic biomarkers, prognostic biomarkers, and treatment targets. Here, we sought to investigate the role and underlying regulatory mechanism of lncRNA small nucleolar RNA host gene 16 ( <i>SNHG16</i>) in CRC. The expressions of <i>SNHG16</i> in CRC were identified by RNA-sequencing and quantitative reverse transcription PCR. The functions of <i>SNHG16</i> were explored by a series of <i>in vitro</i> and <i>in vivo</i> assays (colony formation assay, flow cytometry assay, and xenograft model). Bioinformatics analysis, RNA fluorescence <i>in situ</i> hybridization and luciferase reporter assay were used to investigate the regulatory mechanism of effects of <i>SNHG16</i>. <i>SNHG16</i> was found to be significantly elevated in human CRC tissues and cell lines. Functional studies suggested that <i>SNHG16</i> promoted CRC cell growth both <i>in vitro</i> and <i>in vivo</i>. Mechanistically, we identified that <i>SNHG16</i> is expressed predominantly in the cytoplasm. <i>SNHG16</i> could interact with miR-214-3p and up-regulated its target ABCB1. This study indicated that <i>SNHG16</i> plays an oncogenic role in CRC, suggesting it could be a novel biomarker and therapeutic target in CRC.