Oksidatif Strese Kar？？ 3,4-Dhpea'n？n Koruyucu Etkisinin Modülasyonunda Pten'in Rolü

Prostate cancer (PCa) with a Phosphate tensin homolog (PTEN) gene mutation can become aggressive. In this study, it was hypothesized that the PTEN mutational status in PCa cell lines might modify the chemopreventive effect of 3,4-dihydroxyphenyl ethanol (3,4-DHPEA), thus, determining the cells’ ability to manage oxidative stress created by N,N,N′ ,N′ -Tetrakis(2- pyridylmethyl)ethylenediamine (TPEN). The human PCa cell lines with varying PTEN status, DU-145 (PTEN +/？), 22Rv1 (PTEN +/+), and PC3 (PTEN ？/？), were treated with up to 100 μM of 3,4-DHPEA and/or up to 6.5 μM of TPEN for 24 hours. The viability of cells after treatment was measured with Cell Titer-Glo Luminescent Assay and analyzed with the analysis of variance test. 3,4-DHPEA treatment as high as 50 μM had the greatest cytotoxic effect on 22Rv1 followed by DU-145 and PC3. Similar overall trend was also observed with TPEN treatment. When the cells were treated with TPEN at IC50 doses, 3,4-DHPEA co-treatment still showed cytotoxicity in the same order as 3,4-DHPEA treatment alone. No chemoprotective effect due to 3,4- DHPEA was observed. The data is still consistent with the hypothesis that oxidative stress inducing agents are dependent on the PTEN status. This is consistent with 22Rv1 with wild type PTEN showing the greatest susceptibility to 3,4-DHPE