CEBPG demonstrates oncogene functions and modulates the expression of genes involved in cervical cancer related pathways.

Cervical cancer is a major cause of female cancer incidence and mortality globally. Targeted therapy shows promise with higher efficacy and fewer side effects, yet effective biomarkers are needed. CEBPG, a bZIP transcription factor, has attracted attention as a potential biomarker and therapeutic target. It promotes tumor growth in various cancers, but its role in cervical cancer is unclear. The aim of this study is to investigate the expression, biological function, and transcriptional regulatory mechanisms of CEBPG in cervical cancer. This study analyzed CEBPG expression in cervical cancer using The Cancer Genome Atlas (TCGA) data, overexpressed it in HeLa cells, and conducted proliferation, apoptosis, migration, and invasion experiments. RNA sequencing (RNA-seq) revealed CEBPG's transcriptional regulatory network. Our findings revealed that CEBPG expression was significantly higher in cervical cancer than in normal tissues. Overexpression of CEBPG in HeLa cells significantly enhanced proliferation, migration, and invasion while repressing apoptosis. RNA-seq analysis identified numerous differentially expressed genes (DEGs) enriched in pathways critical for tumorigenesis and progression, such as angiogenesis, cell proliferation, and migration. Bioinformatics analysis identified 27 potential transcriptional targets of CEBPG, several of which were associated with poor prognosis and higher expression in cervical cancer tissues. CEBPG may contribute to malignant phenotypes in cervical cancer, potentially through the transcriptional regulation of specific target genes. The high expression of CEBPG in cervical cancer and its demonstrated role in promoting malignancy through transcriptional regulation provide novel insights into the molecular mechanisms of cervical carcinogenesis and progression. This offers directions for further exploration of CEBPG as a potential therapeutic target and biomarker.