Fig. 6

NF-κB activity is partially involved in the chemoresistance induced by high RAC3 expression levels: a HCT 116 control or shRAC3 cells were co-transfected with κB-Luc reporter plasmid plus RSV-β Gal. Cells were pre-stimulated for 30 min with 0.5 mM SSZ or DMSO, prior to treatment with 3.5 μM FUra or 0.4 μM Oxa for 24 h. The diagram bars correspond to the average ± S.D. of relative light units normalized with the corresponding β-galactosidase values, *p < 0.01 HCT 116 shRAC3 treated with 3.5 μM FUra respect to HCT 116 shRAC3 basal and ***p < 0.001 HCT 116 control treated with drugs respect to HCT 116 control basal, HCT 116 control treated with FUra or Oxa plus SSZ respect to HCT 116 control without SSZ and HCT 116 shRAC3 respect to HCT 116 control. b, c HCT 116 cell lines were pre-stimulated for 30 min with 0.5 mM SSZ and then the cells were treated for 6 h with 3.5 μM FUra or 0.4 μM Oxa. b Representative microphotography (200×) of apoptotic Ethidium Bromide (EtBr) stained cells after 6 h of treatment and c Diagram bars correspond to the percentage of EtBr positive cells per field (at least 10 fields per sample), *p < 0.05 HCT 116 control or shRAC3 FUra plus SSZ respect to HCT 116 treated with FUra and HCT 116 shRAC3 Oxa plus SSZ respect to shRAC3 Oxa, **p < 0.01 HCT 116 control FUra + SSZ respect to HCT 116 control basal and HCT 116 shRAC3 FUra respect to HCT 116 hsRAC3 basal, ***p < 0.001 HCT 116 control Oxa + SSZ respect to HCT 116 control basal and Oxa, HCT 116 shRAC3 FUra + SSZ or Oxa + SSZ respect to HCT 116 shRAC3 treated with FUra or Oxa, respectively