ArticleInternational journal of general medicine2023
Decreased Expression of GLYATL1 Predicts Poor Prognosis in Patients with Clear Cell Renal Cell Carcinoma.
Article in International journal of general medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Integration of a glutamine metabolism-based prognostic signature and a synergistic nanotherapeutic strategy targeting metabolic vulnerabilities in prostate cancer.Discover oncology · 2026Article
- Identification and validation of glucose metabolism-related gene signature in endometrial cancer.BMC cancer · 2025Article
- Identification of glutamine metabolism-related gene signature to predict colorectal cancer prognosis.Journal of Cancer · 2024Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: GLYATL1 is a member of the glycine-N-acyltransferase family, which catalyses acyl group transfer. The role of GLYATL1 in cancer is largely unknown; therefore, the potential value of GLYATL1 in clear cell renal cell carcinoma (ccRCC) was explored. Methods: The ccRCC gene expression profiles and clinical data were obtained from the University of California Santa Cruz Xena platform. Differential expression and survival analysis were performed using R software. Samples from the TIMER public database and real-world were used for validation. The potential molecular mechanism of GLYATL1 in ccRCC was explored using gene set enrichment analysis (GSEA). Results: GLYATL1 was downregulated, indicating a poor prognosis in ccRCC. Low expression of GLYATL1 was significantly associated with advanced stage and higher histological grade ccRCC. The differential expression of GLYATL1 was validated at the protein level using clinical samples and tissue microarray. The results of GSEA showed that multiple crucial signalling pathways including fatty acid metabolism, adipogenesis, oxidative phosphorylation and epithelial-mesenchymal transition were enriched. Conclusion: This study demonstrated that GLYATL1 downregulation has an unfavourable impact on the survival of patients with ccRCC. The resulting data indicated that GLYATL1 could be a potential new target for ccRCC therapy, which may be helpful for the personalized treatment of such individuals.
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