This study investigates the role of AP1S1 in cervical cancer progression using SiHa cervical cancer cells as a model system. We performed quantitative proteomic profiling to identify AP1S1-regulated proteins and downstream signaling pathways. Mechanistically, AP1S1 interacts with HOXC4 to suppress TRIM23-mediated ubiquitination of COX5B, thereby enhancing oxidative phosphorylation and promoting tumor cell proliferation and migration. The raw proteomics data are being deposited to support the findings of this study and to enable further re-analysis by the research community.