In the present study, we report for the first time that ectopic expression of FBXO22 promoted cell viability and inhibited apoptosis in CC cells via promoting the ubiquitination and proteasomal degradation of p57Kip2 uncovering a new mechanism by which FBXO22 promotes malignant properties of cervical cancer (Supplementary Fig. 9). Here, CDKN1C is linked to cervical carcinoma.