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This study aimed to investigate the relationship between  ZNF582  promoter methylation ( ZNF582 m) level and radiosensitivity of cervical cancer and its biological basis. This was a prospective multicenter clinical study, comprising two independent cohorts of locally advanced cervical cancer patients. Exfoliated cervical cells were collected at 0, 24, 30, 36, 48, and 64 Gy to test  ZNF582 mlevels. Radiotherapy response was evaluated according to RECIST Version. RT-PCR and WT were used to detect the mRNA and protein expression levels; MTT and flow cytometry were used to detect the cell viability and cell cycle, respectively. While clone formation and subcutaneous tumorigenesis in nude mice were used to detect the growth of HeLa cells with/without  ZNF582  overexpression. In the first cohort, 22 cases achieved complete remission (CR) or partial response (PR), and the other 28 cases exhibited stable disease (SD). Radiotherapy reduced  ZNF582 mlevels among all patients. Initial lever of  ZNF582 mwas significantly higher in the Responder (CR + PR) group than in the SD group. Also, patients with higher initial lever  ZNF582 mwere more sensitive towards radiotherapy than  ZNF582 m-lowpatients. The second cohort confirmed the above results. The amplitude of  ZNF582 mlevels were related to the radiotherapeutic response; some patients of  ZNF582 m-lowshowed a transient increase in  ZNF582 m, and present greater radiosensitivity than other  ZNF582 m-lowpatients. In vitro, ZNF582 protein overexpression promoted cell cycle arrest in S phase. These results suggested that higher  ZNF582 mlevels predicted greater radiosensitivity in clinical cervical cancer cases. Overexpressed ZNF582 conferred radioresistance by cell cycle arrest in vitro.

epigenetics

ZNF582  promoter methylation predicts cervical cancer radiosensitivity and ZNF582 protein overexpression reduces radiosensitivity by cell cycle arrest in S phase