Hydrogen sulfide lowers proliferation and induces protective autophagy in colon epithelial cells
Open accessAbstract
Hydrogen sulfide (H(2)S) is a gaseous bacterial metabolite that reaches high levels in the large intestine. In the present study, the effect of H(2)S on the proliferation of normal and cancerous colon epithelial cells was investigated. An immortalized colon epithelial cell line (YAMC) and a panel of colon cancer cell lines (HT-29, SW1116, HCT116) were exposed to H(2)S at concentrations similar to those found in the human colon. H(2)S inhibited normal and cancerous colon epithelial cell proliferation as measured by MTT assay. The anti-mitogenic effect of H(2)S was accompanied by G(1)-phase cell cycle arrest and the induction of the cyclin-dependent kinase inhibitor p21(Cip). Moreover, exposure to H(2)S led to features characteristic of autophagy, including increased formation of LC3B(+) autophagic vacuoles and acidic vesicular organelles as determined by immunofluorescence and acridine orange staining, respectively. Abolition of autophagy by RNA interference targeting Vps34 or Atg7 enhanced the anti-proliferative effect of H(2)S. Further mechanistic investigation revealed that H(2)S stimulated the phosphorylation of AMP-activated protein kinase (AMPK) and inhibited the phosphorylation of mammalian target of rapamycin (mTOR) and S6 kinase. Inhibition of AMPK significantly reversed H(2)S-induced autophagy and inhibition of cell proliferation. Collectively, we demonstrate that H(2)S inhibits colon epithelial cell proliferation and induces protective autophagy via the AMPK pathway.
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Several animal and human studies suggest that postprandial hyperglycemia is responsible for initiating esophageal mucosal injury and the development of dysmotility.
“Several animal and human studies suggest that this is responsible for initiating esophageal mucosal injury and the development of dysmotility [13], [18], [19].”
From Cytoprotective Effects of Hydrogen Sulfide in Novel Rat Models of Non-Erosive Esophagitis (2014) · cites this paper as [19]
The Discussion (page unavailable) concerns hydrogen sulfide and colon epithelial cells, not postprandial hyperglycemia or esophageal injury. Searches for the claim’s distinctive terms and for esophageal motility found no passage in our copy addressing that proposed relationship. (LLM, conf=0.78)
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- Authors
- Wu, Y. C., Wang, X. J., Yu, L., Chan, F. K. L., Cheng, A. S. L., Yu, J., Sung, J. J. Y., Wu, W. K. K., & Cho, C. H.
- Affiliations
- Chinese University of Hong Kong (HK)
- Corresponding author
- Wu, William K. K.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-05-29
- Volume
- 7
- Issue
- 5
- Pages
- e37572
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3362591
- OpenAlex
- W2088784248
- Cited by
- 109
- References
- 26
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 5 · 2023: 7 · 2022: 9 · 2021: 13 · 2020: 11 · 2019: 8 · 2018: 11 · 2017: 6 · 2016: 7 · 2015: 8 · 2014: 8 · 2013: 6
- FWCI
- 3.01
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Sulfur Compounds in Biology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Physical Sciences › Engineering › Mechanical Engineering › Catalysis and Hydrodesulfurization Studies
- Keywords
- hydrogen sulfide, colonic epithelial cells, colon cancer, cell proliferation, autophagy, AMPK signaling, mTOR, S6 kinase, p21, G1 cell cycle arrest, Vps34, ATG7, LC3B
- MeSH terms
- Autophagy-Related Protein 7, Animals, Autophagy, Cell Cycle, Cell Line, Cell Movement, Colon, Epithelial Cells, Humans, Hydrogen Sulfide, Intestinal Mucosa, Microtubule-Associated Proteins, Phagosomes, Signal Transduction, Ubiquitin-Activating Enzymes, Cell Proliferation, Cyclin-Dependent Kinase Inhibitor p21, Mice, AMP-Activated Protein Kinases, Class III Phosphatidylinositol 3-Kinases, TOR Serine-Threonine Kinases
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