Long Noncoding RNA CBR3-AS1 Promotes Stem-like Properties and Oxaliplatin Resistance of Colorectal Cancer by Sponging miR-145-5p.

Abstract

Accumulating articles indicate that long noncoding RNAs (lncRNAs) serve as essential regulators in a plethora of human cancers. In this study, we analyzed the expression profile and functional role of lncRNA CBR3-AS1 in colorectal cancer (CRC). High-expression levels of CBR3-AS1 were found in CRC tissues and cell lines. Upregulated CBR3-AS1 was closely associated with poor prognosis and adverse clinicopathological features of CRC patients. Artificial knockdown of CBR3-AS1 markedly suppressed the proliferation, migration, invasion, and stem-like properties but promoted the apoptosis of CRC cells. Moreover, we observed that CBR3-AS1 could directly bind to miR-145-5p and negatively regulated its expression in CRC. Further experiments also demonstrated that inhibition of miR-145-5p reverted the effects of CBR3-AS1 knockdown on CRC cells. In addition, compared with the parental cells, CBR3-AS1 expression was strikingly increased in oxaliplatin- (OXA-) resistant CRC cells, and the OXA resistance was notably diminished by CBR3-AS1 knockdown. To conclude, our study suggested that CBR3-AS1 serves an oncogenic role in CRC and may be exploited as a novel therapeutic target for CRC patients.