Visfatin/eNampt is a novel
adipokine, secreted by visceral and subcutaneous fat, which could be involved in the development of
obesity-associated
cancer. Only few studies revealed
reactive oxygen species (ROS)-dependent action of
visfatin in endothelial cells, myotubes and
melanoma cells. The potential pro-apoptotic properties of
visfatin/eNampt in human colorectal HCT-116 cells remain unknown. The aim of the study was to examine the effects of
visfatin/eNampt on cell viability along with the determination of apoptosis/
necrosis extent and ROS level in HCT-116 cells. Additionally
antioxidant enzymes' activities (i.e
catalase (CAT), gluthatione
peroxidase (GSH-Px)), and lipid peroxidation intensity in HCT-116 cells line was evaluated. Viability of HCT-116 cells was decreased after
visfatin/eNampt treatment for 24 hours. The number of apoptotic cells in tested cells treated with increasing
visfatin/eNampt concentrations (10, 100, 250 ng/ml) was elevated compared to untreated cells (6.4%, 9.7%, 16% vs. 3.2%; respectively). After 24 hours in the
visfatin/eNampt treated group (10 - 100 ng/ml) CAT and GSH-Px activities significantly increased and this observation was accompanied by the decrease of ROS level when compared to the control group. Interestingly ROS level (using DCF detection technique) and lipid peroxidation ratio were increased in cells stimulated by
visfatin/eNampt in concentration of 250 ng/ml along with the decreased activity of selected
antioxidant enzymes when compared to remaining study groups, including control. We concluded that
visfatin/eNampt induces decrease of cell viability and apoptosis boost in human
colorectal cancer HCT-116 cells line.
Visfatin/eNampt affected the level of ROS as well as
antioxidant capacity, however the association of ROS level and apoptosis rate was not linear. The role for
visfatin/eNampt in
cancer redox status in vitro may provide a greater insight into the association between fat derived
visfatin/eNampt and its endocrine action in
colorectal carcinoma cells.