Additional file 1: of SOX17 overexpression sensitizes chemoradiation response in esophageal cancer by transcriptional down-regulation of DNA repair and damage response genes

Table S1. The primers used in the current study. Table S2. Antibodies and their reaction conditions. Table S3. SOX17 binding sites in promoter of DNA repair genes and putative DNA damage response genes in the current study. Figure S1. Knockdown of SOX17 sustained the cell viability upon cisplatin treatment in the KYSE510 and KYSE170 cells. (A, D) RT-qPCR showed low SOX17 mRNA expression upon si-knockdown of SOX17 (si-SOX17) in KYSE510 cells (A) or KYSE170 cells (D). (B, E) Western blots confirmed low SOX17 protein expression in si-SOX17 KYSE510 cells (B) or KYSE170 cells (E). β-actin was used as an internal control. (C, F) Knockdown of SOX17 sustained cell viability upon cisplatin treatment measured by MTT assay in si-SOX17 KYSE510 cells (C) or KYSE170 cells (F). The relative cell viability was normalized to si-control (siCtrl) group. Data represent mean ± SD from three independent experiments. P-values were determined by two-tailed Student’s t-test. *P < 0.05; **P < 0.01; ***P < 0.001. Figure S2. Overexpression of SOX17 in KYSE510-R-SOX17 cells reduced the protein expression level of DNA repair and damage-responsive genes analyzed as compared to KYSE510-R-EV cells. β-actin was used as an internal control for western blots. (PDF 688 kb