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Allicin inhibits the growth of HONE-1 and HNE1 human nasopharyngeal carcinoma cells by inducing ferroptosis
Xin Li1, Jin-Que Luo1, Xue-Qi Liao1
1Hunan Provincial Key Laboratory of the Research and Development of Novel Pharmaceutical Preparations, College of Pharmacy, Changsha Medical University, Changsha, China.
Abstract:
Allicin (AL) is one of garlic-derived organosulfides and has a variety of pharmacological effects. Studies have reported that AL has notable inhibitory effects on liver cancer, gastric cancer, breast cancer, and other cancers. However, there are no relevant reports about its role in human nasopharyngeal carcinoma. Ferroptosis is an iron-dependent form of non-apoptotic regulated cell death. Increasing evidence indicates that induction of ferroptosis can inhibit the proliferation, migration, invasion, and survival of various cancer cells, which act as a tumor suppressor in cancer. In this study, we confirmed that AL can inhibit cell proliferation, migration, invasion, and survival in human nasopharyngeal carcinoma cells. Our finding shows that AL can induce the ferroptosis axis by decreasing the level of GSH and GPX4 and promoting the induction of toxic LPO and ROS. AL-mediated cytotoxicity in human nasopharyngeal carcinoma cells is dependent on ferroptosis. Therefore, AL has good anti-cancer properties and is expected to be a potential drug for the treatment of nasopharyngeal carcinoma.
Insights
Allicin, a compound from garlic, effectively inhibits human nasopharyngeal carcinoma by inducing ferroptosis, a cell death pathway. This suggests allicin is a promising candidate for nasopharyngeal cancer treatment.
Area of Science:
- Oncology
- Biochemistry
- Pharmacology
Background:
- Allicin (AL), a garlic-derived organosulfide, exhibits diverse pharmacological effects, including anti-cancer properties against various tumors.
- Ferroptosis, an iron-dependent cell death, is recognized for its tumor-suppressive role by inhibiting cancer cell proliferation, migration, invasion, and survival.
- The role of allicin in human nasopharyngeal carcinoma and its potential to induce ferroptosis remain largely unexplored.
Purpose of the Study:
- To investigate the effects of allicin on human nasopharyngeal carcinoma cells.
- To determine if allicin-induced cytotoxicity is mediated by ferroptosis.
- To explore the underlying molecular mechanisms of allicin's anti-cancer activity in nasopharyngeal carcinoma.
Main Methods:
- Cell proliferation, migration, and invasion assays were performed on human nasopharyngeal carcinoma cells treated with allicin.
- Levels of glutathione (GSH) and glutathione peroxidase 4 (GPX4) were measured.
- Lipid peroxidation (LPO) and reactive oxygen species (ROS) levels were assessed to evaluate ferroptosis induction.
Main Results:
- Allicin significantly inhibited cell proliferation, migration, and invasion in human nasopharyngeal carcinoma cells.
- Allicin treatment led to decreased levels of GSH and GPX4, key components of the ferroptosis pathway.
- Increased levels of toxic LPO and ROS were observed, indicating the induction of ferroptosis by allicin.
- Allicin-mediated cytotoxicity was confirmed to be dependent on ferroptosis induction.
Conclusions:
- Allicin demonstrates significant anti-cancer properties against human nasopharyngeal carcinoma.
- Allicin induces cell death in nasopharyngeal carcinoma by promoting ferroptosis through the modulation of GSH, GPX4, LPO, and ROS.
- Allicin holds potential as a therapeutic agent for treating nasopharyngeal carcinoma.
