Circular RNAs (circRNA) have been shown to be involved in the pathogenesis of colorectal cancer (CRC). CircCTNNA1 was found to be one of the upregulated circRNAs in CRC. However, there are few studies on circCTNNA1, so it is necessary to carry out further studies. The expression of circCTNNA1, microRNA (miR)-363-3p, and chemokine C-X-C motif ligand 5 (CXCL5) was detected by quantitative real-time PCR (qRT-PCR). The protein levels of CXCL5 and metastasis markers were measured using western blot (WB) analysis. Cell proliferation, apoptosis, cell cycle, migration, and invasion were determined by cell counting kit 8 (CCK8) assay, colony formation assay, flow cytometry, and transwell assay. The relationship between miR-363-3p and circCTNNA1 or CXCL5 was evaluated via dual-luciferase reporter assay and RNA immunoprecipitation assay. Animal study was performed to explore the function of circCTNNA1 on CRC tumorigenesis. CircCTNNA1 and CXCL5 were highly expressed in CRC. Knockdown of circCTNNA1 could inhibit the proliferation, cell cycle, metastasis, and promote the apoptosis of CRC cells. MiR-363-3p could be sponged by circCTNNA1, and the inhibition effect of circCTNNA1 silencing on CRC progression could be reversed by miR-363-3p inhibitor. Moreover, miR-363-3p could interact with CXCL5, and CXCL5 overexpression also could reverse the suppressive effect of miR-363-3p on CRC progression. Downregulation of circCTNNA1 also could hinder the tumor growth of CRC in vivo. CircCTNNA1 enhanced CRC progression via regulating the miR-363-3p/CXCL5 axis.

中文翻译：

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CircCTNNA1充当miR-363-3p的ceRNA，通过促进CXCL5表达促进结直肠癌的发展

环状RNA（circRNA）已被证明与大肠癌（CRC）的发病机理有关。发现CircCTNNA1是CRC中上调的circRNA之一。但是，关于circCTNNA1的研究很少，因此有必要进行进一步的研究。通过定量实时PCR（qRT-PCR）检测到circCTNNA1，microRNA（miR）-363-3p和趋化因子CXC基序配体5（CXCL5）的表达。使用蛋白质印迹（WB）分析测量CXCL5和转移标志物的蛋白质水平。细胞增殖，凋亡，细胞周期，迁移和侵袭通过细胞计数试剂盒8（CCK8）测定，集落形成测定，流式细胞术和transwell测定来确定。miR-363-3p与circCTNNA1或CXCL5之间的关系通过双荧光素酶报告基因分析和RNA免疫沉淀分析进行了评估。进行了动物研究以探索circCTNNA1在CRC肿瘤发生中的功能。CircCTNNA1和CXCL5在CRC中高表达。敲除circCTNNA1可抑制CRC细胞的增殖，细胞周期，转移并促进其凋亡。circCTNNA1可以抑制miR-363-3p的表达，而miR-363-3p抑制剂可以逆转circCTNNA1沉默对CRC进程的抑制作用。而且，miR-363-3p可以与CXCL5相互作用，而CXCL5的过表达也可以逆转miR-363-3p对CRC进展的抑制作用。circCTNNA1的下调也可能阻碍体内CRC的肿瘤生长。CircCTNNA1通过调节miR-363-3p / CXCL5轴增强了CRC进程。敲除circCTNNA1可抑制CRC细胞的增殖，细胞周期，转移并促进其凋亡。circCTNNA1可以抑制miR-363-3p的表达，而miR-363-3p抑制剂可以逆转circCTNNA1沉默对CRC进程的抑制作用。而且，miR-363-3p可以与CXCL5相互作用，而CXCL5的过表达也可以逆转miR-363-3p对CRC进展的抑制作用。circCTNNA1的下调也可能阻碍体内CRC的肿瘤生长。CircCTNNA1通过调节miR-363-3p / CXCL5轴增强了CRC进程。敲除circCTNNA1可以抑制CRC细胞的增殖，细胞周期，转移并促进其凋亡。circCTNNA1可以抑制miR-363-3p的表达，而miR-363-3p抑制剂可以逆转circCTNNA1沉默对CRC进程的抑制作用。而且，miR-363-3p可以与CXCL5相互作用，而CXCL5的过表达也可以逆转miR-363-3p对CRC进展的抑制作用。circCTNNA1的下调也可能阻碍体内CRC的肿瘤生长。CircCTNNA1通过调节miR-363-3p / CXCL5轴增强了CRC进程。miR-363-3p可以与CXCL5相互作用，而CXCL5的过表达也可以逆转miR-363-3p对CRC进展的抑制作用。circCTNNA1的下调也可能阻碍体内CRC的肿瘤生长。CircCTNNA1通过调节miR-363-3p / CXCL5轴增强了CRC的进展。miR-363-3p可以与CXCL5相互作用，而CXCL5的过表达也可以逆转miR-363-3p对CRC进展的抑制作用。circCTNNA1的下调也可能阻碍体内CRC的肿瘤生长。CircCTNNA1通过调节miR-363-3p / CXCL5轴增强了CRC进程。