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DNAJC9, an HSP40 family member with histone chaperone function, exhibits unclear roles in cervical cancer. DNAJC9 is specifically overexpressed in malignant cervical cancer cells, and downregulation of DNAJC9 inhibits proliferation, induces G1/S arrest, and suppresses tumorigenicity. GLI1 has been identified as a key downstream effector of DNAJC9, and GLI1 rescue reverses proliferation defects. Mechanistically, DNAJC9 promotes the p300-H3 interaction to sustain H3K27ac at the GLI1 enhancer and facilitate GLI1 transcription, driving proliferation. Furthermore, DNAJC9 expression correlates positively with GLI1 in clinical specimens, suggesting that the DNAJC9-GLI1 axis is a potential prognostic marker and therapeutic target.
Xie et al. (Thu,) studied this question.