Quinalizarin Triggers U251 Glioma Cell Apoptosis By Inhibiting Phosphatidylinositol 3-Kinase/Protein Kinase B/Mammalian Target Of Rapamycin Signaling Pathway

We have explored whether quinalizarin could trigger human U251 glioma cell mortality and the mechanism(s) therein. Quinalizarin in a dose- and time-dependent manner activated caspase-3 and reduced cyclin-D1 activity in human 251 glioma cells. We observed that quinalizarin downregulated PI3K/Akt/mTOR signaling cascade that further resulted in stimulation of caspase-3 and suppression of the PI3I/Akt signaling cascade. These findings also revealed an increased caspase-3 activation, release of lactic dehydrogenase, and breakdown of Poly (ADP-ribose) polymerase with SH-6 [(2R)-2-methoxy-3-octadecoxypropyl] (2,3,4-trihydroxycyclohexyl) hydrogen phosphate, which is a protein kinase B inhibitor. Co-treatment with quinalizarin and LY294002/SH-6 exhibited enhanced glioma cell apoptosis. Overall the findings advocate protective effect of quinalizarin in U251 glioma cells via inhibition of the PI3K/Akt/mTOR signaling cascade.