Quinacrine inhibits GSTA1 activity and induces apoptosis through G(1)/S arrest and generation of ROS in human non-small cell lung cancer cell lines

Background: Quinacrine (QC) is popular for its anti-malarial activity. It has been reported exhibiting anti-cancerous properties by suppressing nuclear factor-κB and activating p53 signaling; however, its effect on cellular pathways in human non-small cell lung cancer (NSCLC) has not been studied. Materials and Methods: Binding of QC with GSTA1 was studied computationally as well as through GST activity assay kit. Cell viability, cell cycle and mitochondrial membrane potential activity were studied using flow cytometry. RT-PCR and western blot were carried out to understand the involvement of various genes at their mRNA as well as protein level. Results: QC inhibited the activity of GSTA1 approximately by 40–45% which inhibits cell survival and promotes apoptosis. QC reduced viability of NSCLC cells in a dose-dependent manner. It also causes nuclear fragmentation, G(1)/S arrest of cell cycle and ROS generation; which along with disruption of mitochondrial membrane potential activity leads to apoptotic fate. Conclusions: Results revealed, QC has promising anti-cancer potential against NSCLC cells via inhibition of GSTA1, induction of G(1)/S arrest and ROS mediated apoptotic signaling.