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Medical ozone induces proliferation and migration inhibition through ROS accumulation and PI3K/AKT/NF-κB suppression
1Division of Vascular and Interventional Radiology, Department of General Surgery, Nanfang Hospital, Southern Medical University, 1838 Guangzhou Avenue North, Guangzhou, 510515, Guangdong, People's Republic of China.
Background:
Hepatocellular carcinoma is one of the most common malignancies and leading cancer-associated deaths worldwide. Ozone has been proposed as a promising therapeutic agent in the treatment of various disorders.
Purpose:
The purpose of this paper is to assess the potential anticancer effects of the ozone on liver cancer cells.
Method:
The liver cancer cell line of bel7402 and SMMC7721 was used in this study. Proliferation was evaluated using the CCK-8 and the colony formation assay. Wond healing assay and transwell assay without Matrigel were used to evaluate their migration ability. Flow cytometry was used for cell cycle analysis and reactive oxygen species (ROS) determination. Glutathione detection kit was used for measurement of glutathione level. Protein expression was estimated by western blot analysis.
Results:
Ozone treatment inhibited liver cancer cell proliferation, colony formation. Ozone induced G2/M phase cell cycle arrest, which could be elucidated by the change of protein levels of p53, p21, Cyclin D1, cyclin B1, cdc2, and CDK4. We also found that ozone treatment inhibited migration ability by inhibiting EMT-relating protein. Ozone also induced ROS accumulation and decreased glutathione level decreased, which contributed to the inactivation of the PI3K/AKT/NF-κB pathway. Finally, we found that pre-treatment of liver cancer cells with N-acetylcysteine resisted ozone-induced effects.
Conclusions:
Ozone restrains the proliferation and migration potential and EMT process of liver cancer cells via ROS accumulation and PI3K/AKT/NF-κB suppression.
Insights
Ozone therapy shows promise in fighting liver cancer by inhibiting cancer cell growth and migration. It works by increasing reactive oxygen species (ROS) and suppressing key cell signaling pathways.
Area of Science:
- Oncology
- Biochemistry
- Cell Biology
Background:
- Hepatocellular carcinoma is a major global health concern, causing significant mortality.
- Ozone is being explored for its therapeutic potential across various medical conditions.
Purpose of the Study:
- To investigate the anticancer effects of ozone on liver cancer cells.
- To understand the underlying mechanisms of ozone's action.
Main Methods:
- Utilized bel7402 and SMMC7721 liver cancer cell lines.
- Assessed proliferation, colony formation, migration, cell cycle, and reactive oxygen species (ROS).
- Measured glutathione levels and analyzed protein expression via Western blot.
Main Results:
- Ozone inhibited liver cancer cell proliferation and colony formation.
- Ozone induced G2/M phase cell cycle arrest and suppressed epithelial-mesenchymal transition (EMT).
- Ozone increased ROS, decreased glutathione, and inactivated the PI3K/AKT/NF-κB pathway.
Conclusions:
- Ozone restrains proliferation, migration, and EMT in liver cancer cells.
- These effects are mediated by ROS accumulation and PI3K/AKT/NF-κB pathway suppression.
- N-acetylcysteine pre-treatment reversed ozone's effects, confirming the role of ROS.
