This study showed that the overexpression of hsa_circ_0000231 could increase the expression of CCND2 at both mRNA and protein levels, while the knockdown of hsa_circ_0000231 exhibited a reverse effect, thus validating the crosstalk between hsa_circ_0000231 and CCND2. Furthermore, these effects could be partially abolished by miR-375 mimics or inhibitors, hence supporting the hypothesis that hsa_circ_0000231 functioned as a ceRNA to promote CCND2-mediated proliferation via decoying miR-375 in CRC. This evidence concerns the gene CCND2 and colorectal carcinoma.