The Apoptotic Effects of the P300 Activator on Breast Cancer and Lung Fibroblast Cell Lines

Background: p300 is an enzyme that acetylates histones during stress. it alsoacetylates several non-histone proteins, including p53 which is the most important tumorsuppressor gene. p53 plays an important role in the apoptosis of tumor cells. hereby,this study describes the potency of cholera toxin b subunit as a p300 activator to induceapoptosis in a breast cancer cell line (mcf-7) and a lung fibroblast cell line (mrc-5)as a non-tumorigenic control sample. methods: mcf-7 and mrc-5 were cultured in rpmi-1640 and treated with orwithout cholera toxin b subunit at the concentration of 85.43 ?mol/l, based on the half-maximal inhibitory concentration index at different times (24, 48 and 72 h). thepercentage of apoptotic cells was measured by flow cytometry. real-time quantitativert-pcr was performed to estimate the mrna expression of p300 in mcf-7 and mrc-5 with cholera toxin b subunit at different times. we used the elisa and bradford proteintechniques to detect levels of total and acetylated p53 protein generated in mcf-7 andmrc-5. results: our findings indicated that the cholera toxin b subunit effectively andsignificantly induced more apoptosis in mcf-7 compared to mrc-5. we showed thatexpression of p300 up-regulated by increasing the time of the cholera toxin b subunittreatment in mcf-7 but not in mrc-5. in addition, the acetylated and total p53protein levels increased more in mcf-7 cells than in mrc-5 cells.conclusion: cholera toxin b subunit induced significant cell death in mcf-7, butit could be well tolerated in mrc-5. therefore, cholera toxin b subunit can besuggested as an anti-cancer agent.