CircPACRGL promoted cell proliferation, migration and invasion as well as inhibited cell apoptosis in colorectal cancer via regulation of the miR-330-3p/CNBP axis.

Abstract

CircRNAs are a member of noncoding RNAs and have been verified to play an important regulatory role in cancers. In CRC, the regulatory mechanisms of various circRNAs have not been elucidated. The expression of circPACRGL and miR-330-3p was detected with qRT-PCR. The protein expression of CDK4, MMP-9, Bcl-2, Bax, cellular nucleic acid-binding protein (CNBP) and β-actin was measured with western blot. Cell proliferation was analyzed using MTT assay, colony formation assay, and EDU assay. Cell apoptosis was detected using flow cytometry. Cell migration and invasion were measured with wound healing and transwell invasion assay. Luciferase reporter assay and RIP assay was used to determine the relationship of among miR-330-3p, circPACRGL and CNBP in CRC cells. In this study, we found that circPACRGL and CNBP expressed high and miR-330-3p expressed low in CRC tissues and cells. Functional experiments showed that inhibition of circPACRGL reduced cell proliferation, migration and invasion in CRC. In addition, knockdown of circPACRGL contributed to cell apoptosis in CRC. Dual-luciferase report assay determined that circPACRGL was a miR-330-3p sponge molecular and CNBP was a target of miR-330-3p. Reversed experiments showed that the effects of sh-circPACRGL transfection on CRC cells were rescued by up-regulating CNBP expression. In this study, we for the first time found a novel regulatory network of circPACRGL in CRC. The results manifested that circPACRGL affected tumor growth by targeting miR-330-3p/CNBP axis in CRC, highlighting the potential of circPACRGL as a therapeutic target for colorectal cancer.