We aimed to investigate the role of NSUN7 in the progression of Cervical Cancer through a combination of bioinformatics analysis and cell and animal culture experiments. We comprehensively assessed the expression levels of NSUN7 in the TCGA and CCLE databases, and explored its correlations with clinicopathological features, immune cell infiltration, DNA damage repair gene function, drug sensitivity, and methylation status. The NSUN7 gene was disrupted through lentiviral infection, and the effects on cell proliferation, invasion, and apoptosis were evaluated using CCK-8 assay, Transwell migration assay, and flow cytometry analysis. Gene enrichment analysis wasidentify the biological pathways associated with NSUN7 and cervical cancer development. Additionally, a xenograft model of cervical cancer was established to assess the in vivo inhibitory effect of NSUN7 and its impact on pathway molecules. The results of both in vitro and in vivo experiments confirmed that silencing the NSUN7 gene significantly inhibited the growth, spread, and metastasis of cervical cancer cells, while promoting apoptosis. TUNEL assay and HE staining further verified the apoptotic effect of NSUN7 on tumor tissues, and KEGG enrichment analysis revealed a significant enrichment of NSUN7 in the ErbB pathway. Silencing of NSUN7 resulted in a significant down-regulation of key ErbB pathway proteins (HER2, STAT5, PI3K/p-PI3K) as demonstrated by quantitative real-time PCR and Western blot. These findings suggest that NSUN7 may affect the biological behavior of cervical cancer cells and promote tumor development by activating the ErbB signaling pathway.