Circular RNA NOX4 promotes the development of colorectal cancer via the microRNA4855p/CKS1B axis.
2020
Colorectal cancer (CRC) is a common malignancy globally. The aim of the present study was to explore the role and the working mechanism of circular RNA NADPH oxidase 4 (circNOX4; circBase ID, hsa_circ_0023990) in CRC. Reverse transcriptionquantitative (RTq)PCR was used to examine the expression of circNOX4, NOX4 mRNA and microRNA (miR)4855p in CRC tissues and cell lines. 3(4,5Dimethylthiazol2yl)2,5diphenyltetrazolium bromide and Transwell assays were performed to analyze CRC cell viability and motility. The glycolytic ability of CRC cells was assessed by measuring glucose consumption, lactate production, extracellular acidification and O2 consumption rates using commercial kits. The starBase database was used to predict the targets of circNOX4 and miR4855p, and the interaction was confirmed by dualluciferase reporter and RNA immunoprecipitation assays. A murine xenograft model was established to verify the role of circNOX4 in CRC in vivo. The results demonstrated that the expression of circNOX4 was upregulated in CRC tissues and cell lines compared with that in adjacent normal tissues and a normal colon epithelial cell line, respectively. The expression of circNOX4 was negatively associated with the prognosis of patients with CRC. CircNOX4 silencing suppressed the proliferation, migration, invasion and glycolysis of CRC cells. miR4855p was identified as a target of circNOX4. CircNOX4 promoted CRC progression by sponging miR4855p. miR4855p was demonstrated to bind to the 3' untranslated region (UTR) of CDC28 protein kinase regulatory subunit 1B (CKS1B). miR4855p overexpressionmediated malignant properties of CRC cells were partly reversed by the transfection with the CKS1B overexpression plasmid. CircNOX4 silencing restrained the CRC xenograft growth in vivo. Collectively, the results of the present study demonstrated that circNOX4 may serve an oncogenic role in CRC by promoting the proliferation, migration, invasion and glycolysis of CRC cells via the miR4855p/CKS1B axis.
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