ArticleMolecular oncology2020
Characterization of PHGDH expression in bladder cancer: potential targeting therapy with gemcitabine/cisplatin and the contribution of promoter DNA hypomethylation.
Article in Molecular oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Targeting serine synthesis pathway to reverse paclitaxel resistance in NSCLC with combination of paclitaxel and anlotinib.Journal of experimental & clinical cancer research : CR · 2026Article
- PHGDH at the crossroads: metabolic plasticity, metastatic paradoxes, and therapeutic reconnaissance in cancer.Journal of biomedical science · 2026Review
- The "serine code" of metabolic reprogramming: multidimensional roles of the serine synthesis pathway in tumors and novel breakthroughs for targeted therapy.Frontiers in immunology · 2026Review
- Serine metabolism reprogramming in cancer: a multi-tiered regulatory framework.Acta biochimica et biophysica Sinica · 2025Review
- Blood metabolites and gastric cancer risk: A bidirectional 2-sample Mendelian randomization study.Medicine · 2025Article
- Long non-coding RNA MINCR silencing contributes to suppressed gemcitabine resistance in bladder cancer by blocking the ZEB1/PHGDH axis through microRNA-876-5p up-regulation.Journal of molecular histology · 2025Article
- YY2 mediates transcriptional repression of PHGDH and expedites oxidative stress in retinal pigment epithelial cells in diabetic retinopathy.Journal of diabetes investigation · 2025Article
- Recent progress in serine metabolism reprogramming in tumors and strategies for serine deprivation.Frontiers in oncology · 2025Review
- Epigenetic modifications in bladder cancer: crosstalk between DNA methylation and miRNAs.Frontiers in immunology · 2025Review
- Targeting metabolic reprogramming to overcome drug resistance in advanced bladder cancer: insights from gemcitabine- and cisplatin-resistant models.Molecular oncology · 2024Article
- PHGDH: a novel therapeutic target in cancer.Experimental & molecular medicine · 2024Review
- Cellular Responses Induced by NCT-503 Treatment on Triple-Negative Breast Cancer Cell Lines: A Proteomics Approach.Biomedicines · 2024Article
- Participation of protein metabolism in cancer progression and its potential targeting for the management of cancer.Amino acids · 2023Review
- The Differential Metabolic Response of Oral Squamous Cell Carcinoma Cells and Normal Oral Epithelial Cells to Cisplatin Exposure.Metabolites · 2022Article
- DNA Methylation Malleability and Dysregulation in Cancer Progression: Understanding the Role of PARP1.Biomolecules · 2022Review
- microRNA-99a-5p induces cellular senescence in gemcitabine-resistant bladder cancer by targeting SMARCD1.Molecular oncology · 2022Article
- The role of serine metabolism in lung cancer: From oncogenesis to tumor treatment.Frontiers in genetics · 2022Review
- Quantitative ubiquitylomics reveals the ubiquitination regulation landscape in oral adenoid cystic carcinoma.Bioscience reports · 2021Article
- Overexpression of SHMT2 Predicts a Poor Prognosis and Promotes Tumor Cell Growth in Bladder Cancer.Frontiers in genetics · 2021Article
- New insights into molecules and pathways of cancer metabolism and therapeutic implications.Cancer communications (London, England) · 2021Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
d-3-Phosphoglycerate dehydrogenase (PHGDH) conducts an important step in the synthesis of serine. Importantly, the PHGDH gene is often amplified in certain cancers. Our previous studies revealed that PHGDH gene amplification was associated with poor overall survival in clear cell renal cell carcinoma (ccRCC) and that metabolic reprogramming of serine synthesis through PHGDH recruitment allowed ccRCC cells to survive in unfavorable environments. There have been no investigations of the role of PHGDH expression in bladder cancer (BC). In this investigation, we examined the clinical importance of PHDGH in BC. Furthermore, we asked whether PHGDH expression could be exploited for BC therapy. Finally, we investigated the regulatory mechanisms that modulated the expression of PHGDH. Using data from The Cancer Genome Atlas, we found that patients with high-grade BC had significantly higher PHGDH expression levels than did those with low-grade BC. In addition, patients with high PHGDH expression did not survive as long as those with low expression. PHGDH downregulation by si-RNAs or an inhibitor in BC cell lines significantly inhibited proliferative ability and induced apoptosis. Furthermore, combined treatment using a PHGDH inhibitor and gemcitabine/cisplatin achieved synergistic tumor suppression compared to use of a single agent both in vitro as well as in vivo. Mechanistic analyses of PHGDH regulation showed that PHGDH expression might be associated with DNA copy number and hypomethylation in BC. These findings suggest novel therapeutic strategies could be used in BC. Finally, our data enhance our understanding of the role of PHGDH in BC.
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