Quinalizarin exerts an anti-tumour effect on lung cancer A549 cells by modulating the Akt, MAPK, STAT3 and p53 signalling pathways

Quinalizarin may be a potential chemical agent for cancer therapy, as it exerts anti-tumour effects against a variety of different types of cancer. However, the underlying regulatory mechanism and signalling pathways of quinalizarin in lung cancer cells remains unknown. The present study sought to investigate the effects of quinalizarin on proliferation, apoptosis and reactive oxygen species (ROS) generation in lung cancer. MTT assays were used to evaluate the effects of quinalizarin on the viability of lung cancer A549, NCI-H460 and NCI-H23 cells. Flow cytometry was employed to evaluate the effects of quinalizarin on the cell cycle, apoptosis and ROS generation in A549 cells. Western blotting was performed to detect cell cycle and apoptosis-associated protein expression levels in A549 cells. Quinalizarin inhibited A549, NCI-H460 and NCI-H23 cell proliferation and induced A549 cell cycle arrest at the G(0)/G(1) phase. Quinalizarin induced apoptosis by upregulating the expression of B-cell lymphoma 2 (Bcl-2)-associated agonist of cell death, cleaved-caspase-3 and cleaved-poly (adenosine diphosphate-ribose) polymerase, and downregulating the expression of Bcl-2. Furthermore, quinalizarin activated mitogen-activated protein kinase (MAPK) and p53, and inhibited the protein kinase B and signal transducer and activator of transcription-3 (STAT3) signalling pathways. In addition, quinalizarin increased ROS generation. The ROS scavenger N-acetyl-L-cysteine restored quinalizarin-induced cell apoptosis, and inactivated the MAPK and STAT3 signalling pathways. The results of the present study demonstrated that quinalizarin induces G(0)/G(1) phase cell cycle arrest and apoptosis via ROS mediated-MAPK and STAT3 signalling pathways.