CDCA8 promotes the proliferation and migration of cervical cancer through regulating CDK1

Cervical cancer (CC) is the 4th most common female cancer globally. Although its overall incidence rate has been declining for decades, the occurrence of advanced diseases and cervical adenocarcinoma (usually undetectable by cytology) are increasing. Therefore, predictors and therapeutic targets for CC are urgently required. Cell division cycle-associated 8 (CDCA8) has been observed to participate in mitotic regulation as a component of the chromosomal passenger complex. Furthermore, the activity of cancer-related CDCA8 hyperactivation has been comprehensively studied; however, its association and underlying molecular mechanism in CC remain elusive. Therefore, this study investigated the association of CDCA8 with CC and revealed that CDCA8 is significantly overexpressed in CC patients and related to poor clinical prognosis. Moreover, CDCA8 knockdown using small hairpin RNA (shRNA) inhibited the CC cell line’s proliferation and migration, as well as enhanced apoptosis. In addition, CDCA8 knockdown was also related to reduced tumor growth in the mouse CC model. RNA sequencing and co-immunoprecipitation assay revealed that CDCA8 interacted with cyclin-dependent kinase 1 (CDK1). The study also observed that CDK1 overexpression inhibited the suppressive effect of CDCA8 knockdown on CC cell growth and migration. In summary, this study indicated that the CDCA8/CDK1 axis plays an essential carcinogenic role in CC, thereby providing a potential novel target for CC diagnosis and treatment.