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Stevioside induced cytotoxicity in colon cancer cells via reactive oxygen species and mitogen-activated protein kinase signaling pathways-mediated apoptosis
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- Published online on: February 14, 2017 https://doi.org/10.3892/ol.2017.5744
- Pages: 2337-2343
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Copyright: © Ren et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
The role of mitogen-activated protein kinase (MAPK) signaling pathways in cell growth and differentiation has been well established. The present study aimed to investigate the anti‑proliferative effect of stevioside on human colon cancer HT‑29 cells. Additionally, the effect of stevioside on cell cycle arrest and MAPK signaling pathways in HT‑29 cells was explored. Stevioside was observed to significantly inhibit cancer cell growth at a dose of 5 µM at 48 and 72 h. A dose‑dependent increase in the apoptosis rate was observed with cell cycle arrest at G2/M phase. In addition, caspase-9 and caspase-3 activity also increased. An increase in reactive oxygen species (ROS) production and a decrease in the mitochondrial membrane potential indicated that the mitochondrial‑mediated intrinsic pathway is responsible for apoptotic activity. These results were additionally verified by the elevated expression level of phosphorylated p38 and extracellular signal‑regulated kinase mitogen‑activated protein kinases (MAPKs). Additionally, by inhibiting ROS production and MAPK activation, the antiproliferative effect of stevioside was suppressed, confirming the hypothesis that ROS and MAPK proteins induce apoptosis in human colon cancer HT-29 cells.