Xu Ma1, Chong Deng2. 1. Department of Colorectal Anorectal Surgery, The First People's Hospital of Jingmen, Jingmen, 448000, Hubei, China. 2. Department of Gastrointestinal Surgery, The First People's Hospital of Jingmen, No.168 Xiangshan Avenue, Jingmen, 448000, Hubei, China. cwovsrl@163.com.
Abstract
BACKGROUND: Cancer progression can be regulated by noncoding circular RNAs. A recent study has indicated that circ_0044556 facilitated the progression of colorectal cancer. AIM: This research was performed to explore the regulatory mechanism of circ_0044556 in CRC. METHODS: Circ_0044556, miR-665 and Diaphanous Homolog 1 levels were detected by the quantitative real-time polymerase chain reaction. Cell proliferation analysis was performed by cell counting kit-8 assay and Edu assay. Cell cycle progression was assessed using flow cytometry. The protein examination was conducted using western blot. Transwell assay was used to analyze cell migration and invasion. Dual-luciferase reporter assay was performed to validate the interaction between targets. In vivo research was implemented by xenograft tumor assay. RESULTS: Circ_0044556 was upregulated in colorectal cancer samples and cells. Silencing circ_0044556 inhibited cell proliferation, cell cycle progression, migration, invasion, and epithelial-mesenchymal transition in CRC cells. Circ_0044556 could directly target miR-665 and the function of circ_0044556 was associated with the regulation of miR-665. In addition, Diaphanous Homolog 1 was a target gene for miR-665 and the anti-tumor role of miR-665 in colorectal cancer was dependent on the downregulation of Diaphanous Homolog 1. Diaphanous Homolog 1 level was regulated by circ_0044556 via sponging miR-665 in CRC cells. In vivo assay suggested that circ_0044556 promoted CRC tumor growth by regulating the miR-665 and Diaphanous Homolog 1 levels. CONCLUSION: Our findings manifested that circ_0044556 functioned as an oncogenic circRNA in colorectal cancer by mediating the miR-665/Diaphanous Homolog 1 axis, elucidating the molecular mechanism of circ_0044556 in CRC progression.
BACKGROUND: Cancer progression can be regulated by noncoding circular RNAs. A recent study has indicated that circ_0044556 facilitated the progression of colorectal cancer. AIM: This research was performed to explore the regulatory mechanism of circ_0044556 in CRC. METHODS: Circ_0044556, miR-665 and Diaphanous Homolog 1 levels were detected by the quantitative real-time polymerase chain reaction. Cell proliferation analysis was performed by cell counting kit-8 assay and Edu assay. Cell cycle progression was assessed using flow cytometry. The protein examination was conducted using western blot. Transwell assay was used to analyze cell migration and invasion. Dual-luciferase reporter assay was performed to validate the interaction between targets. In vivo research was implemented by xenograft tumor assay. RESULTS: Circ_0044556 was upregulated in colorectal cancer samples and cells. Silencing circ_0044556 inhibited cell proliferation, cell cycle progression, migration, invasion, and epithelial-mesenchymal transition in CRC cells. Circ_0044556 could directly target miR-665 and the function of circ_0044556 was associated with the regulation of miR-665. In addition, Diaphanous Homolog 1 was a target gene for miR-665 and the anti-tumor role of miR-665 in colorectal cancer was dependent on the downregulation of Diaphanous Homolog 1. Diaphanous Homolog 1 level was regulated by circ_0044556 via sponging miR-665 in CRC cells. In vivo assay suggested that circ_0044556 promoted CRC tumor growth by regulating the miR-665 and Diaphanous Homolog 1 levels. CONCLUSION: Our findings manifested that circ_0044556 functioned as an oncogenic circRNA in colorectal cancer by mediating the miR-665/Diaphanous Homolog 1 axis, elucidating the molecular mechanism of circ_0044556 in CRC progression.