Fig. 7.

HSP90 inhibitor 17-AAG exhibits similar effects as knockdown of PGK1. a-b. MTT assay was used to evaluate the effects of HSP90 inhibitor 17-AAG on cell viability in endometrial cell lines Ishikawa (a) and HEC1A (b). DMSO was used as negative control. c. Western blot was used to detect the expression of DNA repair-related proteins c-JUN, FOSL1, and POLD1 in the presence of HSP90 inhibitor 17-AAG in Ishikawa cancer cell line. β-actin was used as a loading control. d. Semi-quantitative analysis of protein level in C. e. Western blot was used to detect the expression of DNA repair-related proteins c-JUN, FOSL1, and POLD1 in the presence of HSP90 inhibitor 17-AAG in HEC1A cancer cell line. β-actin was used as a loading control. f. Semi-quantitative analysis of protein level in E. g. Western blot was performed to examine the effect of HSP90 inhibitor 17-AAG on the expression of DNA methyltransferases (DNMT1, DNMT3A, and DNMT3B) and SPARC in Ishikawa cancer cell line. β-actin was used as a loading control. h. Semi-quantitative analysis of protein level in G. i. Western blot was performed to examine the effect of HSP90 inhibitor 17-AAG on the expression of DNA methyltransferases (DNMT1, DNMT3A, and DNMT3B) and SPARC in HEC1A cancer cell line. β-actin was used as a loading control. j. Semi-quantitative analysis of protein level in I. Data were shown as mean ± SD based on three independent experiments. *, P < 0.05, **, P < 0.01 compared with DMSO group