Low Concentration Cisplatin Treatment Leads to an Epithelial Mesenchymal Transition-like Response in DU 145 Prostate Cancer Cells

Prostate cancer is the second most frequently diagnosed cancer and the sixth leading cause of cancer death(Jemal et al., 2011). Its incidence is higher in developed countries, in America it is the most common cancer and is the second leading cause of cancer death in men (Siegel et al., 2014). In Asia, its incidence is relatively low, but shows a increasing trend (Jung et al., 2013; Du et al., 2014). Although multiple approaches has been used to treat this cancer, 10-25% prostate cancer patients still die of , mainly cancer metastasis (D’Amico et al., 2002). Cisplatin is a commonly used chemotherapeutic drug for varied types of cancers including prostate cancer. It kills cancer cells by covalently binding to DNA and forming DNA adducts, which activates various signaltransduction pathways, such as DNA-damage recognition and repair, cell-cycle arrest, and programmed cell death/ apoptosis (Siddik, 2003; Kelland, 2007). It has been reported that the residual ovarian cells that survived 3 or 5 days of cisplatin treatment display EMT and stem cell properties including increased invasiveness(Latifi et al., 2011; Baribeau et al., 2014), And the MAPK/ERK signaling pathway activation was reported to be one of the possible mechanisms underlying cisplatin’s this effect (Baribeau et al., 2014). Similar to this