ArticleInternational journal of biological sciences2023
LncRNA UCA1 Participates in De Novo Synthesis of Guanine Nucleotides in Bladder Cancer by Recruiting TWIST1 to Increase IMPDH1/2.
Article in International journal of biological sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Integrated assessment of non-invasive diagnostic tools for bladder cancer: a network meta-analysis.Frontiers in oncology · 2025Pooled it
- LncRNA PCAT7 drives tumorigenesis and glycolytic reprogramming in breast cancer via the ceRNA-mediated miR-204-5p/RUNX2 axis.Cancer gene therapy · 2026Article
- Genomic diversification between aposematic and cryptic phenotypes of Oophaga granulifera (Anura: Dendrobatidae).Scientific reports · 2026Article
- IMP metabolic mechanisms and IMPDH targeting strategies in tumor metabolic reprogramming and therapy (Review).International journal of molecular medicine · 2026Review
- The integration of transcriptomics and metabolomics elucidates the antitumor mechanisms of mycophenolic acid in bladder cancer cells.BMC cancer · 2025Article
- Approaches for Identifying LncRNA-Associated Proteins for Therapeutic Targets and Cancer Biomarker Discovery.Targets (Basel) · 2025Article
- Identification of a cuproptosis‑related prognostic biomarker and therapeutic target in ovarian cancer.Oncology letters · 2025Article
- IMPDH2's Central Role in Cellular Growth and Diseases: A Potential Therapeutic Target.Cell proliferation · 2025Review
- Crosstalk between RNA-binding proteins and non-coding RNAs in tumors: molecular mechanisms, and clinical significance.International journal of biological sciences · 2025Review
- Construction of a disulfidptosis-associated lncRNA signature to predict prognosis in bladder cancer.Translational andrology and urology · 2024Article
- Integrative analysis of toxicometabolomics and toxicoproteomics data: new molecular insights into thiazolidinedione-induced cardiotoxicity.Metabolomics : Official journal of the Metabolomic Society · 2024Article
- Potential role of TWIST1 and its methylation in bladder urothelial carcinoma.Translational cancer research · 2024Article
- Huaier inhibits cholangiocarcinoma cells through the twist1/FBP1/Wnt/β-catenin axis.Molecular biology reports · 2024Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic dysregulation has been identified as one of the hallmarks of cancer biology. Based on metabolic heterogeneity between bladder cancer tissues and adjacent tissues, we discovered several potential driving factors for the bladder cancer occurrence and development. Metabolic genomics showed purine metabolism pathway was mainly accumulated in bladder cancer. Long noncoding RNA urothelial carcinoma-associated 1 (LncRNA UCA1) is a potential tumor biomarker for bladder cancer diagnosis and prognosis, and it increases bladder cancer cell proliferation, migration, and invasion via the glycolysis pathway. However, whether UCA1 plays a role in purine metabolism in bladder cancer is unknown. Our findings showed that UCA1 could increase the transcription activity of guanine nucleotide de novo synthesis rate limiting enzyme inosine monophosphate dehydrogenase 1 (IMPDH1) and inosine monophosphate dehydrogenase 2 (IMPDH2), triggering in guanine nucleotide metabolic reprogramming. This process was achieved by UCA1 recruiting the transcription factor TWIST1 which binds to the IMPDH1and IMPDH2 promoter region. Increased guanine nucleotide synthesis pathway products stimulate RNA polymerase-dependent production of pre-ribosomal RNA and GTPase activity in bladder cancer cells, hence increasing bladder cancer cell proliferation, migration, and invasion. We have demonstrated that UCA1 regulates IMPDH1/2-mediated guanine nucleotide production via TWIST1, providing additional evidence of metabolic reprogramming.
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