Hydrogen Gas Stops Gastric Cancer Cell Growth in Lab Study
- Authors
- Baocheng Zhu, Hengguan Cui, Weiqiang Xu
- Journal
- Cancer Cell International
- Year
- 2021
- DOI
- 10.1186/s12935-020-01743-5
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Gastric Cancer
- Body System
- Digestive System
TL;DR
Hydrogen gas treatment may offer a new way to slow down the growth and spread of gastric cancer by affecting certain molecules in the cancer cells.
Key Finding
Hydrogen gas significantly inhibited gastric cancer cell proliferation and migration in laboratory studies and tumor growth in mice, working through a specific molecular pathway involving three regulatory molecules.
Summary
Researchers tested whether hydrogen gas could slow the growth of gastric (stomach) cancer cells in laboratory dishes and in mice. They found that hydrogen gas reduced cancer cell growth and movement, and it did this by changing the activity of certain molecules (called lncRNA MALAT1, miR-124-3p, and EZH2) that control how cancer cells behave. When they artificially increased one of these molecules (MALAT1), hydrogen's anti-cancer effects disappeared, suggesting this molecular pathway is key to how hydrogen works.
Practical Takeaway
While these results are promising, this study was conducted only in laboratory cells and mice—not in humans. Much more research, including human clinical trials, would be needed before hydrogen gas could be considered a gastric cancer treatment. The findings do suggest a potential mechanism worth investigating further, but anyone with gastric cancer should rely on established medical treatments rather than hydrogen-based approaches.
Abstract
Background: Gastric cancer is one of the most prevalent and deadly malignancies without efficient treatment option. This study aimed to investigate the effect of hydrogen gas on the behavior of gastric cancer cells. Methods: Gastric cancer cell lines MGC-803 and BGC-823 were treated with or without H2 /O2 gas mixture (66.7%:33.3% v/v). Proliferation and migration were assessed by MTT and scratch wound healing assays respectively. The expression of lncRNA MALAT1, miR-124-3p, and EZH2 was analyzed by real-time quantitative PCR and/or western blot. Tumor growth was estimated using xenograft mouse model. Results: H2 gas significantly inhibited gastric tumor growth in vivo and the proliferation, migration, and lncRNA MALAT1 and EZH2 expression of gastric cancer cells while upregulated miR-124-3p expression. LncRNA MALAT1 overexpression abolished all the aforementioned effects of H2. LncRNA MALAT1 and miR-124-3p reciprocally inhibited the expression of each other. MiR-124-3p mimics abrogated lncRNA MALAT1 promoted EZH2 expression and gastric cancer cell proliferation and migration. Conclusions: These data demonstrated that H2 might be developed as a therapeutics of gastric cancer and lncRNA MALAT1/miR-124-3p/EZH2 axis could be a target for intervention.