Journal of gastrointestinal oncology · 2026
Helicobacter pylori-induced cystathionine-γ-lyase drives redox imbalance and metabolic remodeling in gastric cancer.
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Wang Yangyang, Xu Ruixue, Wang Ziqi, Wu Yufei, Han Shuyi, Zhang Xi, Li Huanjie
Аннотация
BACKGROUND: Helicobacter pylori (H. pylori) infection is a major risk factor for gastric cancer (GC) and depends on nutrient and energy metabolism, particularly amino acids, for colonization. In host cells, cysteine is regulated by the transsulfuration (TSS) pathway, in which cystathionine-γ-lyase (CSE) generates cysteine, hydrogen sulfide (H2S), and reactive sulfur species (RSS). Dysregulation of this pathway may contribute to gastric carcinogenesis. This study aims to investigate the role of CSE in H. pylori-associated GC and to characterize the associated alterations in sulfur metabolism and redox regulation.
METHODS: To model the gastric microenvironment during H. pylori infection and dissect the functional role of host CSE, we used in vitro infection models, CSE knockout mice, and metabolic profiling. The use of CSE knockout mice enables specific assessment of host CSE in gastric inflammation and tissue protection, providing a controlled and tractable in vivo system to study host metabolic enzyme function in the context of chronic bacterial infection, which has direct relevance to human gastric pathophysiology. Additionally, we examined the effects of garlic-derived organosulfur compounds, diallyl trisulfide (DATS) on H. pylori colonization, cysteine/TSS metabolism, oxidative stress, and GC cell proliferation.
RESULTS: H. pylori infection upregulated CSE and altered cysteine metabolism, leading to RSS imbalance, pro-tumorigenic signaling, and inflammation. Systemic CSE deficiency in vivo exacerbated gastric inflammatory injury following H. pylori infection, indicating that CSE contributes to host tissue protection under inflammatory conditions. These observations suggest that CSE functions as a metabolic and redox regulator of which its biological impact depends on cellular context, facilitating tumor cell adaptation while preserving host homeostasis during infection.
CONCLUSIONS: Our findings support a role for CSE in the metabolic and redox alterations associated with H. pylori infection and gastric carcinogenesis. The modulation of CSE-related pathways by DATS suggests that sulfur metabolism may represent a relevant area for future mechanistic and translational studies.
METHODS: To model the gastric microenvironment during H. pylori infection and dissect the functional role of host CSE, we used in vitro infection models, CSE knockout mice, and metabolic profiling. The use of CSE knockout mice enables specific assessment of host CSE in gastric inflammation and tissue protection, providing a controlled and tractable in vivo system to study host metabolic enzyme function in the context of chronic bacterial infection, which has direct relevance to human gastric pathophysiology. Additionally, we examined the effects of garlic-derived organosulfur compounds, diallyl trisulfide (DATS) on H. pylori colonization, cysteine/TSS metabolism, oxidative stress, and GC cell proliferation.
RESULTS: H. pylori infection upregulated CSE and altered cysteine metabolism, leading to RSS imbalance, pro-tumorigenic signaling, and inflammation. Systemic CSE deficiency in vivo exacerbated gastric inflammatory injury following H. pylori infection, indicating that CSE contributes to host tissue protection under inflammatory conditions. These observations suggest that CSE functions as a metabolic and redox regulator of which its biological impact depends on cellular context, facilitating tumor cell adaptation while preserving host homeostasis during infection.
CONCLUSIONS: Our findings support a role for CSE in the metabolic and redox alterations associated with H. pylori infection and gastric carcinogenesis. The modulation of CSE-related pathways by DATS suggests that sulfur metabolism may represent a relevant area for future mechanistic and translational studies.