SMC4/SMAD3/NF-κB axis drives cervical cancer progression and radioresistance via DNA damage repair and immune modulation

Our study identifies SMC4 as a regulator that promotes radioresistance and potentially modulates the tumor immune microenvironment in cervical cancer, likely by coordinating DNA damage repair and activating the SMAD3-NF-κB pathway. These findings suggest that SMC4 could be a potential therapeutic target for radiosensitization and a candidate biomarker for patient stratification.