Fig. 13

A model representing the mechanisms of survival, migration, and carboplatin resistance in OVCAR5 CBPR cell line deduced from the identification and validation of differential expressed proteins. Carboplatin resistant OVCAR5 cell line undergoes EMT transformation resulting in less proliferation and energy consumption but are more migratory in phenotype compared to parental cells. Altered metabolism in these cells results in upregulated G6PD expression which drives the pentose phosphate pathway, essential for reprogrammed metabolism and neutralization of increased oxidative stress (ROS) afflicted by carboplatin treatment through maintenance of GSH. Stabilization of ROS through sustenance of GSH is also provided by upregulation of AKR1B1 and GFPT2 expression. In addition, upregulation of TGFBI and related ECM components such as FLNA, ITGAV, ITGA1 and ITGA2 remodels the ECM to sustain chemoresistance and EMT transformation, essential for metastasis and survival of these cells