Artemetin, A Dietary Flavonoid Inhibits the Proliferation and Induces Apoptosis in Human Gastric Carcinoma (AGS) Cells

Abstract: Background: One of the most common types of recurrent carcinoma cases worldwide is gastric cancer. Even advances in treatment methods and early discoveries have not been able to significantly lower the death and morbidity rates associated with gastric cancer. On account of their multiple health benefits, apparent lack of toxicity and side effects, and the limitations of chemotherapeutic drugs, natural products have attracted a lot of interest in recent years with the aim of preventing cancer. Aim: A flavonoid class phytochemical known as Artemetin, has been discovered to be present in numerous medicinal plants. Anti-bacterial, antioxidant, and anti-inflammatory, hepatoprotective and cardioprotective actions are only a few of its many pharmacological effects. Materials and Methods: In the current investigation, the potential of Artemetin as an anticancer agent for gastric cancer was evaluated in AGS cell lines. The influence of Artemetin on the cell viability, apoptotic induction, mitochondrial ATPase activity, ROS generation, and cell cycle progression has been examined. Cisplatin was selected as the positive control for the experiments. Results: The impact of Artemetin on the cell viability revealed that its cytotoxic potential increased in a dose-dependent pattern and IC50 concentrations were chosen for further experiments. The results showed that apoptosis was induced by Artemetin in AGS cells by triggering ROS pathway and DNA damage. The cell viability of AGS cells was reduced with increased concentration of Artemetin. Conclusion: Artemtin's cytotoxic potential in cells is mediated by inducing apoptosis, which is supported by significant levels of ROS and mitochondrial ATPase as well as the findings of the AO/EB staining. All these results suggest that Artemetin can be used as a potent anticancer drug for human gastric carcinoma. Keywords: Gastric cancer, Artemetin, AGS cells, Reactive oxygen species, Apoptosis.