Hydrogen Gas Shrinks Colorectal Cancer Tumors in Lab Study
- Authors
- Xiangyan Zhang, Geru Tao, Ya'nan Zhao, Sijie Xing, Jie Jiang, Boyan Liu, Shucun Qin
- Journal
- BioMed Research International
- Year
- 2022
- DOI
- 10.1155/2022/8024452
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Colorectal Cancer
- Body System
- Digestive System
TL;DR
Breathing in high levels of molecular hydrogen (H2) gas can slow down the growth of colorectal cancer by affecting certain proteins in the cancer cells.
Key Finding
Molecular hydrogen gas reduced colorectal cancer cell growth in the lab and shrank tumors in mice by blocking a protein signaling pathway involved in cancer cell multiplication.
Summary
Researchers tested whether molecular hydrogen (H2, a gas) could slow the growth of colorectal cancer cells and tumors. In laboratory tests, hydrogen reduced cancer cell growth, and in mice with implanted tumors, inhaling hydrogen gas (67% concentration for 2 hours daily) shrank tumors. The researchers found that hydrogen works by blocking a specific protein pathway (called AKT/SCD1) that cancer cells use to multiply.
Practical Takeaway
This is early-stage research conducted only in cells and mice, not in humans. While the results are promising, they do not yet indicate that hydrogen therapy would be effective against colorectal cancer in people. Much more research, including human clinical trials, would be needed before any therapeutic claims could be made.
Abstract
Objective: Molecular hydrogen (H2) has been considered a potential therapeutic target in many cancers. Therefore, we sought to assess the potential effect of H2 on colorectal cancer (CRC) in this study. Methods: The effect of H2 on the proliferation and apoptosis of RKO, SW480, and HCT116 CRC cell lines was assayed by CCK-8, colony formation, and flow cytometry assays. The effect of H2 on tumor growth was observed in xenograft implantation models (inhalation of 67% hydrogen two hours per day). Western blot and immunohistochemistry analyses were performed to examine the expression of p-PI3K, PI3K, AKT, pAKT, and SCD1 in CRC cell lines and xenograft mouse models. The expression of SCD1 in 491 formalin-fixed, paraffin-embedded CRC specimens was investigated with immunochemistry. The relationship between SCD1 status and clinicopathological characteristics and outcomes was determined. Results: Hydrogen treatment suppressed the proliferation of CRC cell lines independent of apoptosis, and the cell lines showed different responses to different doses of H2. Hydrogen also elicited a potent antitumor effect to reduce CRC tumor volume and weight in vivo. Western blot and IHC staining demonstrated that H2 inhibits CRC cell proliferation by decreasing pAKT/SCD1 levels, and the inhibition of cell proliferation induced by H2 was reversed by the AKT activator SC79. IHC showed that SCD1 expression was significantly higher in CRC tissues than in normal epithelial tissues (70.3% vs. 29.7%, p = 0.02) and was correlated with a more advanced TNM stage (III vs. I + II; 75.9% vs. 66.3%, p = 0.02), lymph node metastasis (with vs. without; 75.9% vs. 66.3%, p = 0.02), and patients without a family history of CRC (78.7% vs. 62.1%, p = 0.047). Conclusion: This study demonstrates that high concentrations of H2 exert an inhibitory effect on CRC by inhibiting the pAKT/SCD1 pathway. Further studies are warranted for clinical evaluation of H2 as SCD1 inhibitor to target CRC.