In the study, we found, for the first time to our knowledge, that circCDKN2B-AS1 acted as a promoter that facilitated aerobic glycolysis by sponging IMP3 protein to stabilize HK2 mRNA, consequently promoted malignant phenotypes in cervical cancer in vitro and in vivo, and the synthesizing inhibitory peptide IIP could effectively block the interaction between circCDKN2B-AS1 and IMP3 protein. This evidence concerns the gene IMP3 and cervical carcinoma.