D-Y Ding1, D Wang, Z-B Shu. 1. Department of Gastrointestinal Colorectal Surgery, China-Japan Union Hospital, Jilin University, Changchun, China. zefafw@163.com.
Abstract
OBJECTIVE: Colorectal cancer (CRC) is a common tumor around the world. Circular RNAs (circRNAs) have been reported to be related to the development of CRC. However, the detailed mechanism is complicated. This study aimed to reveal the functional mechanism of circ_0007534 in CRC. PATIENTS AND METHODS: Quantitative real time polymerase chain reation (qRT-PCR) and Western blot assay were performed to analyze gene expression. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and colony formation assay were carried out to determine cell proliferation ability. Furthermore, cell migratory and invasive abilities were assessed by transwell assay. Glycolytic metabolism was examined via the measurements of extracellular acidification rate (ECAR), glucose consumption, and lactate production. Also, the interaction between circ_0007534 or solute carrier family 25 member 22 (SLC25A22) and miR-613 was predicted and confirmed by starBase v2.0 and the Dual-Luciferase reporter assay, respectively. Mouse xenograft was performed to investigate the effect of circ_0007534 on tumor growth in vivo. RESULTS: Circ_0007534 and SLC25A22 levels were upregulated, and miR-613 level was downregulated in CRC tissues/cells. Circ_0007534 knockdown repressed CRC cell proliferation, colony formation, migration, invasion, and glycolysis. Interestingly, Circ_0007534 targeted miR-613, and miR-613 targeted SLC25A22. Circ_0007534 exerted its function by repressing miR-613 expression, and miR-613 exerted its function via inhibiting SLC25A22 expression. Also, Circ_0007534 repressed miR-613 expression to upregulate SLC25A22 level. Circ_0007534 depletion repressed tumor growth in vivo. CONCLUSIONS: We demonstrated that circ_0007534 knockdown suppressed the growth of CRC cells by regulating miR-613/SLC25A22 axis, providing potential target for the treatment of CRC.
OBJECTIVE:Colorectal cancer (CRC) is a common tumor around the world. Circular RNAs (circRNAs) have been reported to be related to the development of CRC. However, the detailed mechanism is complicated. This study aimed to reveal the functional mechanism of circ_0007534 in CRC. PATIENTS AND METHODS: Quantitative real time polymerase chain reation (qRT-PCR) and Western blot assay were performed to analyze gene expression. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and colony formation assay were carried out to determine cell proliferation ability. Furthermore, cell migratory and invasive abilities were assessed by transwell assay. Glycolytic metabolism was examined via the measurements of extracellular acidification rate (ECAR), glucose consumption, and lactate production. Also, the interaction between circ_0007534 or solute carrier family 25 member 22 (SLC25A22) and miR-613 was predicted and confirmed by starBase v2.0 and the Dual-Luciferase reporter assay, respectively. Mouse xenograft was performed to investigate the effect of circ_0007534 on tumor growth in vivo. RESULTS: Circ_0007534 and SLC25A22 levels were upregulated, and miR-613 level was downregulated in CRC tissues/cells. Circ_0007534 knockdown repressed CRC cell proliferation, colony formation, migration, invasion, and glycolysis. Interestingly, Circ_0007534 targeted miR-613, and miR-613 targeted SLC25A22. Circ_0007534 exerted its function by repressing miR-613 expression, and miR-613 exerted its function via inhibiting SLC25A22 expression. Also, Circ_0007534 repressed miR-613 expression to upregulate SLC25A22 level. Circ_0007534 depletion repressed tumor growth in vivo. CONCLUSIONS: We demonstrated that circ_0007534 knockdown suppressed the growth of CRC cells by regulating miR-613/SLC25A22 axis, providing potential target for the treatment of CRC.