• DNAJC9 is overexpressed in malignant cervical cancer cells and its downregulation inhibits proliferation, induces G1/S arrest, and suppresses tumorigenicity.
• GLI1 is a key downstream effector of DNAJC9; GLI1 rescue reverses proliferation defects caused by DNAJC9 knockdown.
• DNAJC9 promotes p300-H3 interaction to sustain H3K27ac at the GLI1 enhancer, facilitating GLI1 transcription.
• DNAJC9 expression positively correlates with GLI1 in clinical specimens, suggesting the DNAJC9-GLI1 axis as a prognostic marker and therapeutic target.