Fig. 8: ZNF202 mediates transcriptional expression of CYLD.

a Total RNA was isolated and subjected to real-time PCR analysis of ZNF202 in EBV-positive (HK1-EBV and HONE1-EBV) cells compared with EBV-negative (HK1 and HONE1) cells. b Total RNA was isolated and subjected to real-time PCR analysis of ZNF202 in radiation-resistant cells (CNE2-IR and HK1-IR) compared with radiation-responsive cells (CNE2 and HK1) cells. c Immunoblot analysis of ZNF202 in EBV-positive (HK1-EBV and HONE1-EBV) cells compared with EBV negative (HK1 and HONE1) cells and ZNF202 protein expression levels in radiation-resistant cells (CNE2-IR and HK1-IR) compared with radiation-responsive cells (CNE2 and HK1) cells. β-Actin was used as a control. HK1-EBV cells transfected with ZNF202 siRNAs: d Cell lysates were then extracted and subjected to Western blotting. β-Actin was used as a control. e total RNA from cells was isolated and subjected to real-time PCR. f The level of ZNF202 binding to the CYLD promoter in HONE1 and HONE1-EBV cells was analyzed by using ChIP followed by RT-PCR of 3 specific regions (n = 3). g Schematic illustration of the CYLD promoter and 3 potential binding sites of ZNF202. h 293 T cells were or were not co-transfected with ZNF202 and the luciferase reporter driven by the wild-type CYLD promoter or mutant CYLD promoter, together with a PLR-TK construct. Results are plotted as the mean surviving fraction ± SEM of 3 independent experiments. i Representative IHC staining of ZNF202 and CYLD expression from pathological sections of nasopharyngeal squamous cell carcinoma patients. j The CYLD protein expression level was calculated according to ZNF202 expression of nasopharyngeal squamous cell carcinoma patients. High- and low-expressing groups were classified according to median score.