Objective In this study, the role and potential mechanism of transformer 213 (Tra213) in cervical cancer were explored.Methods The transcriptional data of Tra213 in patients with cervical cancer from Gene Expression Profiling Interactive Analysis (GEPIA) and cBioPortal databases were investigated. The functions of Tra213 were evaluated by using Western blot, MTT, colony formation, Transwell assays, and nude mouse tumor formation experiments. Target genes regulated by Tra213 were studied by RNA-seq. Subsequently, representative genes were selected for RT-qPCR, confocal immunofluorescence, Western blot, and rescue experiments to verify their regulatory relationship.Results The dysregulation of Tra213 in cervical cancer samples was observed. Tra213 overexpression in Siha and Hela cells enhanced cell viability and proliferation, whereas Tra213 knockdown showed the opposite effect. Alteration of Tra213 expression did not affect cell migration and invasion. Furthermore, tumor xenograft models verified that Tra213 promoted cervical cancer growth. Mechanically, Tra213 positively regulated the mRNA and protein level of SP1, which was critical for the proliferative capability of Tra213.Conclusion This study demonstrated the important role of the Tra213/SP1 axis in the progression of cervical cancer in vitro and in vivo, which provides a comprehensive understanding of the pathogenesis of cervical cancer.