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<p>Gastric cancer (GC) is a significant global health issue, annually affecting approximately one million individuals and causing substantial mortality. Major risk factors, such as Helicobacter pylori infection, influence GC progression through alterations in host immunity and cellular metabolism. Uridine phosphorylase 1 (UPP1) is a key enzyme in pyrimidine nucleoside metabolism and plays an important role in regulating cell proliferation, survival, and cancer metabolism. Our analyses reveal significant dysregulation of UPP1 in GC tissues compared with normal counterparts, suggesting its involvement in tumorigenesis and disease progression. Moreover, <i>H. pylori</i>–induced UPP1 expression is associated with enhanced glycolytic metabolism, potentially facilitating tumor cell proliferation and survival. These findings highlight a H. pylori–NF-κB–UPP1–glycolysis axis that links infection-driven inflammation to metabolic reprogramming in GC. Understanding the mechanistic role of UPP1 may support its development as a biomarker and therapeutic target, with implications for early diagnosis and personalized treatment strategies in GC.</p>

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Helicobacter pylori promotes gastric cancer progression via UPP1-mediated uridine bypass of glycolysis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月22日

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  • Xuyu Chen,
  • Ronghua Lu,
  • Siying Wang,
  • Xin Jiang,
  • Jianlei Xia,
  • Xinyu Fu,
  • Yukun Ping,
  • Min Zhang,
  • Yanbing Ding

摘要

Gastric cancer (GC) is a significant global health issue, annually affecting approximately one million individuals and causing substantial mortality. Major risk factors, such as Helicobacter pylori infection, influence GC progression through alterations in host immunity and cellular metabolism. Uridine phosphorylase 1 (UPP1) is a key enzyme in pyrimidine nucleoside metabolism and plays an important role in regulating cell proliferation, survival, and cancer metabolism. Our analyses reveal significant dysregulation of UPP1 in GC tissues compared with normal counterparts, suggesting its involvement in tumorigenesis and disease progression. Moreover, H. pylori–induced UPP1 expression is associated with enhanced glycolytic metabolism, potentially facilitating tumor cell proliferation and survival. These findings highlight a H. pylori–NF-κB–UPP1–glycolysis axis that links infection-driven inflammation to metabolic reprogramming in GC. Understanding the mechanistic role of UPP1 may support its development as a biomarker and therapeutic target, with implications for early diagnosis and personalized treatment strategies in GC.