Emodin Exhibits Strong Cytotoxic Effect in Cervical Cancer Cells by Activating Intrinsic Pathway of Apoptosis

Abstract

Cervical cancer is widely acknowledged as the main cause of mortality and a major obstacle to increasing life expectancy, after breast cancer, in women. Natural products have been proven to be a promising source for the development of potential anticancer drugs. Emodin (1,3,8-trihydroxy-6-methyl-9,10-anthracenedione) is shown to exert wide range of biol. effects, including antibacterial, hepatoprotective, anti-inflammatory and anticancer. The major aim of this study was to evaluate the efficacy of emodin against the progression of human cervical cancer. The cytotoxic effect of emodin on cervical cancer HeLa cells was assessed by cell viability assay and phase contrast microscopy. Moreover, DAPI staining was performed to analyze nuclear condensation. H2DCFDA staining was done to evaluate ROS generation. Activation of caspases was determined to ascertain mitochondria-mediated apoptosis in cervical cancer cells. The results revealed that emodin strongly inhibited the HeLa cell growth and proliferation; which was validated by cell viability assay and phase contrast microscopy. Moreover, DAPI staining authenticated nuclear condensation and fragmentation in HeLa cells indicating initiation of apoptosis. We also observed significant ROS generation and caspases activation in emodin-treated cervical cancer cells. Our results suggested strong cytotoxic potential of emodin against cervical cancer cells.