Fig 1: The POLI treatment enhanced the radioresistance of esophageal squamous cell carcinoma cells in vitro and in vivo.A ESCC patients were classified into low- and high-POLI expression groups according to IHC scores (IHC score 6 was used as a cutoff value for POLI) in all cases. Scale bar, 50 μm. P value was measured by Student’s t test. B Results recorded from Kaplan-Meier survival analysis for overall survival (OS) and disease-free survival (DFS) revealed significantly shortened OS (P = 0.029) and DFS (P = 0.014) for patients with high POLI expression compared to patients with low POLI expression. C The protein levels of POLI in ESCC and normal cell lines were detected by western blot. D Analysis of POLI expression in the ectopic POLI (TE-1-POLI oe vs TE-1-empty) and specific endogenous POLI knockdown (KYSE-150-shPOLI vs KYSE-150-shNC) ESCC cells using Western blot. E Clonogenic survival curves were generated for TE-1 and KYSE-150 cells that were exposed to 2, 4, 6, and 8 Gy X-ray irradiation. The single hit multiple target radiobiological model was used to fit the survival curves. F Images as well as growth curve of the volume out of ESCC tumor xenografts in nude mice. The tumor volumes were presented as the mean ± SEM of three independent experiments. P value was measured by Student’s t test. G The expression level of Ki67 in tumors from the mice was detected by IHC staining. ***P < 0.00, **P < 0.01.
Fig 2: POLI inhibits ubiquitin-mediated degradation of RAD51 by blocking the interaction between RAD51 and XIAP in a competitive binding manner.A Over-expression of POLI impaired the interaction between XIAP and RAD51 proteins. B Schematic diagram of the POLI protein domains. Characterize the regions of POLI mediating its binding with XIAP. C Schematic diagram of RAD51 protein domains. D Characterize the regions of RAD51 mediating its binding with XIAP. E Schematic diagram of XIAP protein domains. F Identification of the regions of XIAP that mediate its binding with POLI and RAD51.
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