Health & Environmental Research Online (HERO)


Print Feedback Export to File
7053737 
Journal Article 
Hesperidin-triggered necrosis-like cell death in skin cancer cell line A431 might be prompted by ROS mediated alterations in mitochondrial membrane potential 
Zhao, W; Chen, Yu; Zhang, X; , 
2018 
Yes 
International Journal of Clinical and Experimental Medicine
ISSN: 1940-5901 
E-CENTURY PUBLISHING CORP 
MADISON 
1948-1954 
WOS:000429006600061 
Skin cancer is one of the lethal causes of cancer related deaths around the globe and with limited drug options and the side effects associated with the currently used drugs; there is pressing need for identification of novel anticancer lead molecules. The aim of the present study was to evaluate the anticancer activity of hesperidin against skin carcinoma cell line A431 and to investigate the underlying mechanism. IC50 was determined by MTT assay. Fluorescent probes DCFH-DA, Indo 1/AM, DiOC6 were used to determine ROS, Ca2+, mitochondrial membrane potential (Delta psi(m)). ATP levels were determined by using ATP liteTM kit. DNA damage was investigated by DAPI and comet assays. Protien expression was investigated by western blotting. Hesperidin exhibited lowest IC50 of 25 mu M against skin A431 cell line. Moreover, hesperidin reduced the cell viability of A431 cells concentration and time-dependently. It also augmented the discharge of ROS and Ca2+ and lessened the mitochondrial membrane potential (Delta psi(m)) and ATP levels in A431 cells. Additionally, hesperidin also prompted DNA damage in A431 cell line. Notably, hesperidin stimulated the cytochrome c release only and exhibited no effect on the expression of apoptosis-related protein levels such as caspase-3, caspase-8, and Apaf-1. Taken together, hesperidin induced A431 cells death displayed a cellular pattern characteristic of necrotic cell death but not of apoptosis.