Figure 7
PIASγ cDNA-transfected sensitive tumors manifested low ROS up on cisplatin treatment to demonstrate chemoresistance response. (a) Sensitive EAC cells were transfected with empty vector (EAC-V) or vector containing PIASγWT-cDNA (EAC-P) and scored for their sensitivity to cisplatin (10 μM). The effectiveness of PIASγ modification was confirmed by Western blot analysis (inset). (b) Mice implanted with the EAC-V or EAC-P cells were evaluated for change in abdominal perimeter (left panel) and tumor volume (right panel) after treatment with cisplatin. Graphical representation of (c) viable cell count, and (d) percent apoptosis of the EAC-V and EAC-P cells after cisplatin treatment. (e) Histogram overlay (left panel) and graphical representation (right panel) depicting ROS in cisplatin-treated EAC-V or EAC-P tumors. (f) CR-EAC were transfected with the vector containing PIASγCA-cDNA (catalytically inactive form of PIASγ) and scored for their sensitivity to cisplatin (10 μM). (g) Mice implanted with either the CR-EAC cells or the PIASγCA-cDNA-expressing CR-EAC cells were evaluated for change in tumor volume (left panel) and viable cell number (right panel) after treatment with cisplatin. α-actin was used as internal control. Values are mean±S.E.M. of five independent experiments in each case. *P<0.01 when compared with respective untreated/normal sets. Values are mean±S.E.M. of five independent experiments in each case
