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CD90 Promotes Gastric Cancer Progression by Regulating SLC1A5-Mediated Glutamine Metabolism Through YY1
Zihua Zhou1, Siyi Liu2, Chenyu Zhang2
1Department of Oncology, Loudi Central Hospital, Loudi, China.
Cancer Science
|April 1, 2026
Summary
CD90 (THY1) protein enhances gastric cancer progression by altering glutamine metabolism via SLC1A5. This impacts cell proliferation and ferroptosis, offering new insights into cancer pathogenesis.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Metabolism
Background:
- CD90 (THY1) is a cell surface glycoprotein implicated in malignant tumor development.
- It influences tumor cell proliferation, metastasis, angiogenesis, stemness, and metabolism.
- CD90 is a prognostic biomarker, but its role in gastric cancer (GC) glutamine metabolism is unclear.
Purpose of the Study:
- To investigate the role and mechanisms of CD90 in glutamine metabolism in gastric cancer cells.
- To elucidate how CD90 influences GC progression through metabolic pathways.
Main Methods:
- Investigated CD90's effect on glutamine metabolism in GC cells.
- Analyzed the interaction between CD90, YY1, and the SLC1A5 promoter.
- Assessed the impact on SLC1A5 transcription, glutamine metabolism, and ferroptosis.
Main Results:
- CD90 promotes GC progression by affecting glutamine metabolism via SLC1A5.
- CD90 facilitates YY1 binding to the SLC1A5 promoter, increasing its transcriptional level.
- This mechanism influences SLC1A5-mediated glutamine metabolism and ferroptosis in GC cells.
Conclusions:
- CD90 plays a significant role in regulating glutamine metabolism in GC cells.
- The CD90-YY1-SLC1A5 axis promotes GC progression and affects ferroptosis.
- Findings provide evidence for GC pathogenesis and potential therapeutic targets.
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