ArticleCancer science2025
GGCT Inhibits Ferroptosis in PTC Cells by Upregulating p53 Through RPS15A.
Article in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Discovery of a Novel γ-Glutamylcyclotransferase Inhibitor Plumbagin by Luminescence-Based High-Throughput Screening.Cancer science · 2026Article
- Mechanistic insights into ferroptosis in thyroid cancer and its therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026Review
- Article
- The Role of Translation-Associated Proteins in p53 Modulation: Mechanisms and Implications.International journal of molecular sciences · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
γ-Glutamine cyclotransferase (GGCT) is an enzyme involved in the metabolic cycle of glutathione (GSH). Abnormal GSH metabolism is mostly related to ferroptosis. However, the mechanisms supporting aberrant GGCT expression in PTC remain to be investigated. In this study, we found that GGCT knockdown inhibited GSH synthesis and promoted malondialdehyde (MDA) and reactive oxygen species (ROS) accumulation, thereby promoting ferroptosis in papillary thyroid cancer cells. Pro-GA, the specific inhibitor of GGCT, inhibited the subcutaneous tumor formation of K1 cells. IP combined with LC-MS/MS showed an interaction between GGCT and RPS15A. RPS15A is highly expressed in PTC tissues and cells, and GGCT promotes the stability of RPS15A. Knockdown of RPS15A promoted p53 expression, which in turn inhibited SLC7A11 expression, resulting in ferroptosis, while overexpression of RPS15A reversed GGCT-induced ferroptosis. In addition, miR-205-5p targeted the 3' UTR of GGCT to inhibit GGCT-mediated ferroptosis, tumor growth, and lung metastasis. In conclusion, we found that knockdown of GGCT promoted ferroptosis in PTC cells. Mechanistically, GGCT interacts with RPS15A, and GGCT promotes the protein stability of RPS15A. Knockdown of RPS15A promotes p53 expression and inhibits SLC7A11 expression, thereby inhibiting GSH synthesis. The upstream mechanism of GGCT regulation showed that miR-205-5p inhibited GGCT protein expression by targeting the 3' UTR of GGCT.
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