Hydrogen Gas Kills Lung Cancer Cells by Blocking Cell Survival Signals
- Authors
- Leyuan Liu, Zhenfeng Yan, Yuanyuan Wang, Jinghong Meng, Gang Chen
- Journal
- Oncology Letters
- Year
- 2020
- DOI
- 10.3892/ol.2020.11973
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Lung Cancer
- Body System
- Respiratory
TL;DR
Hydrogen gas helps to kill lung cancer cells and increase their self-destruction process by blocking certain cell signals.
Key Finding
Blocking autophagy (a cellular recycling process) enhanced hydrogen gas's ability to kill lung cancer cells in laboratory cultures.
Summary
This laboratory study examined how hydrogen gas affects lung cancer cells grown in culture. Researchers found that hydrogen gas triggered two cellular processes: apoptosis (programmed cell death) and autophagy (a cellular cleanup process). Interestingly, when autophagy was blocked, hydrogen gas became more effective at killing cancer cells, suggesting that blocking autophagy might enhance hydrogen gas's anti-cancer effects.
Practical Takeaway
This is early laboratory research in cancer cells only—not human studies—so it cannot yet inform treatment decisions. The findings suggest a potential strategy of combining hydrogen gas with autophagy-blocking approaches, but much more research in animal models and humans would be needed before any clinical application. Anyone with cancer should consult their oncologist about proven treatments.
Abstract
Our previous study found that hydrogen gas (H2) could efficiently inhibit lung cancer progression; however, the underlying mechanisms still remains to be elucidated. The present study aimed to explore the roles of H2 in lung cancer cell autophagy, and reveal the effects of autophagy on H2-mediated lung cancer cell apoptosis and the underlying mechanisms. The expression levels of proteins associated with cell apoptosis and autophagy were detected using western blot analysis. Cell autophagy was inhibited by 3-methyladenine treatment or Beclin1 downregulation, while rapamycin was used to induce autophagy. Cell growth and apoptosis were detected using the Cell Counting Kit-8 and flow cytometry assays, respectively. The results demonstrated that cell apoptosis and autophagy were significantly enhanced in the A549 and H1975 lung cancer cell lines treated with H2. However, autophagy enhancement weakened H2 roles in promoting cell apoptosis and vice versa. In addition, it was found that H2 treatment induced marked decreases in the protein expression levels of phosphorylated STAT3 and Bcl2, and overexpression of STAT3 abolished H2 roles in promoting cell apoptosis and autophagy. Overall, the present study revealed that H2 can promote lung cancer cell apoptosis and autophagy via inhibiting the activation of STAT3/Bcl2 signaling and suppression of autophagy can enhance H2 roles in promoting lung cancer cell apoptosis.