Akt inhibitor and Tacrolimus arrange apoptotic gene expression levels in MCF7 cells

<p>Apoptosis balances the cells produced as a result of cell division and controls the differentiation in general tissue homeostatic mechanisms. It is known that apoptosis is a gene-oriented program and has effects on cell proliferation and differentiation by regulating several pro-apoptotic and anti-apoptotic gene families<span>.</span>&nbsp;In this study we investigated gene expression levels of tumor suppressor gene <em>p53</em>, survival protein and growth factor receptor <em>PDGFR</em>&beta;, anti-apoptotic protein <em>NF&kappa;</em>&beta;, pro-apoptotic proteins <em>Bax</em> and <em>Caspase 9</em>. According to our gene expression results, we showed that levels of p53, Bax and Caspase 9 in MCF7 cells were increased with Akt inhibitor application. Previous studies have reported that Akt inhibitor induces apoptosis by expressing these genes. Also our NF&kappa;B gene expression results support these findings. This effect of the Akt inhibitor shows that the PI3K/Akt/mTOR signaling pathway is one of the primary effective routes on apoptosis in MCF7 cells. It was observed that FK506 administration with Akt inhibitor contributed positively in favor of apoptosis in all parameters, although alone treatment FK506 showed no&nbsp;increase as Akt inhibitor in p53, Bax and Caspase 9 expression. This effect of FK506 showed that the Calcineurin/NFAT pathway is a secondary effective route on apoptosis. However, this positive effect of the co-administration of FK506 with Akt inhibitor on breast cancer gives us important clues for our subsequent studies. When we evaluated our findings of apoptosis and gene expression, it was observed that the combined treatment of the FK506 and Akt inhibitor, which did not show much effect alone, was highly effective and promising in reducing cancer proliferation and regulating apoptotic genes. These results indicate that the intracellular pathways which are used by the cancer act together and support each other.</p>