Punicalagin induces ROS-mediated apoptotic cell death through inhibiting STAT3 translocation in lung cancer A549 cells.

Lung cancer is a noxious disease with substandard overall survival. Despite this, there are several treatment strategies for lung cancer include chemotherapy, radiotherapy, surgery; however, the overall survival remains poor. Punicalagin has been documented as a potential phytomedicine to selectively inhibit the progression and expansion of numerous cancers. In the present study, we evaluated the antiproliferative ability of punicalagin against lung cancer A549 cells by inducing apoptosis by inhibiting STAT-3 activation. Punicalagin induces toxic effects of A549 cells in a dose-associated manner after 24 h treatment. And we also observed that punicalagin (10, 20, and 30 μM) induced reactive oxygen species generation, alters the mitochondrion membrane potential and apoptotic morphological changes in A549 cells. The STAT-3 overexpression regulates apoptosis, proliferation, and angiogenesis. Here, the punicalagin inhibited STAT-3 translocation and thereby induces apoptosis by inhibiting expression Bcl-2 and enhanced expression of Bax, cytochrome-c, caspase-9, and caspase-3 in A549 cells. Hence, we stated that the punicalagin is a possible therapy for non-small cell lung, malignancies. Altogether, the punicalagin is a promising phytomedicine in malignancy treatment and further endeavors are needed to unveil the complete potential.