Hydrogen Therapy Shrinks Cervical Cancer Tumors in Mouse Study
- Authors
- Jing Chu, Jinghai Gao, Jing Wang, Lingling Li, Guoqiang Chen, Jianhong Dang, Zhifeng Wang, Zhijun Jin, Xiaojun Liu
- Journal
- Oncology Reports
- Year
- 2021
- DOI
- 10.3892/or.2021.8092
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Cervical Cancer
- Body System
- Reproductive System
TL;DR
Hydrogen gas inhalation was found to slow down the growth of cervical cancer cells and tumors by promoting cell death and decreasing stress in cells.
Key Finding
Hydrogen gas inhalation reduced cervical cancer cell growth and increased cancer cell death in laboratory cells and in mice, with the effect linked to suppression of two specific cellular signaling pathways (HIF-1α and NF-κB).
Summary
Researchers tested whether hydrogen gas could slow the growth of cervical cancer cells and tumors in mice. They found that hydrogen gas treatment caused cancer cells to die more readily, slowed their growth, and reduced harmful molecules called reactive oxygen species. The study identified that hydrogen appears to work by turning down two cellular signaling pathways (HIF-1α and NF-κB) that help cancer cells survive and multiply.
Practical Takeaway
This is early laboratory and animal research showing a potential mechanism for how hydrogen might affect cervical cancer—it does not yet demonstrate safety or effectiveness in humans. Before any clinical application could be considered, human studies would be needed to confirm these findings and establish whether hydrogen inhalation could be a viable treatment option.
Abstract
Cervical cancer is considered one of the diseases with the highest mortality among women and with limited treatment options. Hydrogen (H2) inhalation has been reported to have a variety of tumor‑suppressive effects, but the exact mechanism remains unclear. In the present study, HeLa cervical cancer cells and HaCaT keratinocytes treated with H2, and a HeLa xenograft mouse model subjected to H2 inhalation were established. TUNEL, Cell Counting Kit‑8 and Ki67 staining assays were used to detect cell apoptosis and proliferation. Oxidative stress was determined according to the levels of reactive oxygen species, malondialdehyde and superoxide dismutase. Tumor growth was recorded every 3 days, and the excised tumors were stained with hematoxylin and eosin. High‑throughput RNA sequencing and subsequent Gene Ontology (GO) enrichment analysis were performed in HeLa‑treated and un‑treated HeLa cells. The expression of hypoxia‑inducible factor (HIF)‑1α and NF‑κB p65 was verified by western blotting, immunohistochemistry and reverse transcription‑quantitative PCR. The results revealed an increased apoptosis rate, and reduced cell proliferation and oxidative stress in H2‑treated HeLa cells but not in HaCaT cells. Similarly, decreased tumor growth and cell proliferation, and enhanced cell apoptosis were observed in H2‑treated HeLa tumors. RNA sequencing and GO analysis suggest that downregulated HIF1A (HIF‑1α mRNA) and RelA (NF‑κB p65) levels, and reduced NF‑κB signaling were associated with the antitumor effect of H2. Finally, decreased HIF‑1α and NF‑κB p65 expression both at the transcriptional and translational levels were observed in H2‑treated HeLa cells and in HeLa‑derived tumors. In conclusion, the present study reveals a novel mechanism of H2 against cervical cancer, which may serve as a potential therapeutic target in clinical practice.