Hydrogen Gas Blocks Lung Cancer Growth by Targeting Key Protein
- Authors
- Dongchang Wang, Lifei Wang, Yu Zhang, Yunxia Zhao, Gang Chen
- Journal
- Biomedicine & Pharmacotherapy
- Year
- 2018
- DOI
- 10.1016/j.biopha.2018.05.055
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Lung Cancer
- Body System
- Respiratory System
TL;DR
Hydrogen gas (H2) has been found to slow down the growth and spread of lung cancer cells and may offer a new treatment approach.
Key Finding
Hydrogen gas inhibited lung cancer cell growth, migration, and invasion while promoting cancer cell death by reducing levels of the SMC3 protein and halting cells in the G2/M phase of the cell cycle.
Summary
Researchers tested whether hydrogen gas could slow lung cancer growth by studying its effects on cancer cells in the laboratory and in mice. They found that hydrogen gas reduced cancer cell growth, stopped cells from spreading, and triggered cancer cell death by affecting a protein called SMC3 that controls how chromosomes are organized during cell division. In mice with lung cancer, hydrogen gas reduced tumor size, though not as effectively as the chemotherapy drug cisplatin.
Practical Takeaway
This is early laboratory and animal research showing hydrogen gas may have anti-cancer properties against lung cancer through a specific molecular mechanism. However, these findings are from cell cultures and mice, not humans, so it is far too early to draw conclusions about whether hydrogen gas could help treat lung cancer in people. Much more research, including human clinical trials, would be needed before any therapeutic claims could be made.
Abstract
Lung cancer is one of the most common lethal malignancies in the globe. The patients' prognoses are dim due to its high metastatic potential and drug resistance. Therefore, in the present study, we aim to find a more potent therapeutic approach for lung cancer. We mainly explored the function of hydrogen gas (H2) on cell viability, apoptosis, migration and invasion in lung cancer cell lines A549 and H1975 by CCK-8, flow cytometry, wound healing and transwell assays, respectively. We used RNA-seq, qPCR and western blotting to detect the different expression genes (DEGs) between H2 group and control group to find the gene related to chromosome condensation. Besides, we confirmed the structural maintenance of chromosomes 3 (SMC3) and H2 on the progression of lung cancer in vitro and vivo. Results showed that H2 inhibited cell viability, migration and invasion, and catalyzed cell apoptosis and H2 induced A549 and H1975 cells G2/M arrest. Besides, H2 down-regulated the expression of NIBPL, SMC3, SMC5 and SMC6, and also reduced the expression of Cyclin D1, CDK4 and CDK6. H2 translocated the subcellular location of SMC3 during cell division and decreased its stability and increased its ubiquitination in both A549 and H1975 cells. In addition, inhibition of the proliferation, migration and invasion and promotion of the apoptosis of A549 and H1975 cells induced by H2 were all abolished when overexpressed SMC3 in the presence of H2. Animal experimental assay demonstrated that the tumor weight in H2 group was significantly smaller than that in control group, but was bigger than cis-platinum group. The expression of Ki-67, VEGF and SMC3 were decreased when mice were treated with H2 or cis-platinum, especially for cis-platinum. All data suggested that H2 inhibited lung cancer progression through down-regulating SMC3, a regulator for chromosome condensation, which provided a new method for the treatment of lung cancer.