J Dai1, Y Zhuang, M Tang, Q Qian, J-P Chen. 1. Department of Gastroenterology, the Third Affiliated Hospital of Soochow University, Changzhou, P.R. China. jianpingchen361@163.com.
Abstract
OBJECTIVE: The aim of this study is to explore the regulatory mechanism of circRNA UBAP2 (circUBAP2) in colorectal cancer (CRC). PATIENTS AND METHODS: The expression levels of circUBAP2, miR-199a, and VEGFA in tissues and cell lines were detected by RT-qPCR. The cell proliferation was examined by CCK-8 and colony formation assays. The migration and invasion abilities were evaluated by wound healing and transwell assays, respectively. Bioinformatics analysis and Luciferase activity assay were applied to determine the interaction between genes. RESULTS: The expression of circUBAP2 was upregulated in CRC tissues and cell lines, and depletion of circUBAP2 suppressed the cell proliferation, migration, and invasion of CRC. Furthermore, miR-199a inhibitor abrogated the suppressive effect of circUBAP2 knockdown on CRC progression. Vascular endothelial growth factor A (VEGFA) was identified as a downstream target gene of miR-199a, and overexpression of VEGFA rescued the tumor phenotypes attenuated by circUBAP2 knockdown or miR-199a overexpression. CONCLUSIONS: Our findings demonstrated that circUBAP2 facilitated CRC progression by sponging miR-199a to upregulate VEGFA. These findings implied that circUBAP2 may be a potential therapeutic biomarker for CRC.
OBJECTIVE: The aim of this study is to explore the regulatory mechanism of circRNA UBAP2 (circUBAP2) in colorectal cancer (CRC). PATIENTS AND METHODS: The expression levels of circUBAP2, miR-199a, and VEGFA in tissues and cell lines were detected by RT-qPCR. The cell proliferation was examined by CCK-8 and colony formation assays. The migration and invasion abilities were evaluated by wound healing and transwell assays, respectively. Bioinformatics analysis and Luciferase activity assay were applied to determine the interaction between genes. RESULTS: The expression of circUBAP2 was upregulated in CRC tissues and cell lines, and depletion of circUBAP2 suppressed the cell proliferation, migration, and invasion of CRC. Furthermore, miR-199a inhibitor abrogated the suppressive effect of circUBAP2 knockdown on CRC progression. Vascular endothelial growth factor A (VEGFA) was identified as a downstream target gene of miR-199a, and overexpression of VEGFA rescued the tumor phenotypes attenuated by circUBAP2 knockdown or miR-199a overexpression. CONCLUSIONS: Our findings demonstrated that circUBAP2 facilitated CRC progression by sponging miR-199a to upregulate VEGFA. These findings implied that circUBAP2 may be a potential therapeutic biomarker for CRC.