ArticleThe Biochemical journal2005
Cancer cells activate p53 in response to 10-formyltetrahydrofolate dehydrogenase expression.
Article in The Biochemical journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 45 citations in OpenAlex.
- Determinants of CBiomolecules · 2026Article
- Mitochondria-transliterated ALDH1L1 functions as a feedback regulator of redox homeostasis in cancer cells to enhance the resistance to pro-oxidative therapy.Cell death and differentiation · 2026Article
- Clinical implications of 10-formyltetrahydrofolate dehydrogenase expression in hormone receptor-positive breast cancer.Frontiers in oncology · 2026Article
- Probing the metabolic regulator and candidate tumor suppressor ALDH1L1 as a target for non-small cell lung cancer gene therapy.Molecular therapy. Oncology · 2025Article
- Disrupted mitochondrial morphology and function exacerbate inflammation in elderly-onset ulcerative colitis.Immunity & ageing : I & A · 2025Article
- Abnormal downregulation of 10-formyltetrahydrofolate dehydrogenase promotes the progression of oral squamous cell carcinoma by activating PI3K/Akt/Rb pathway.Cancer medicine · 2023Article
- Exploratory Metabolomics Underscores the Folate Enzyme ALDH1L1 as a Regulator of Glycine and Methylation Reactions.Molecules (Basel, Switzerland) · 2022Article
- Structure of putative tumor suppressor ALDH1L1.Communications biology · 2022Article
- Article
- Article
- Loss of ALDH1L1 folate enzyme confers a selective metabolic advantage for tumor progression.Chemico-biological interactions · 2019Review
- The Role of Single-Nucleotide Polymorphisms in the Function of Candidate Tumor Suppressor ALDH1L1.Frontiers in genetics · 2019Review
- Article
- Modeling of interactions between functional domains of ALDH1L1.Chemico-biological interactions · 2017Article
- ALDH1L1 variant rs2276724 and mRNA expression predict post-operative clinical outcomes and are associated with TP53 expression in HBV-related hepatocellular carcinoma.Oncology reports · 2017Article
- CerS6 Is a Novel Transcriptional Target of p53 Protein Activated by Non-genotoxic Stress.The Journal of biological chemistry · 2016Article
- Ceramide Synthase 6 Is a Novel Target of Methotrexate Mediating Its Antiproliferative Effect in a p53-Dependent Manner.PloS one · 2016Article
- Folate stress induces apoptosis via p53-dependent de novo ceramide synthesis and up-regulation of ceramide synthase 6.The Journal of biological chemistry · 2013Article
- Molecular mechanisms underlying the potentially adverse effects of folate.Clinical chemistry and laboratory medicine · 2013Review
- Decreased expression of ALDH1L1 is associated with a poor prognosis in hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
A folate enzyme, FDH (10-formyltetrahydrofolate dehydrogenase; EC 1.5.1.6), is not a typical tumour suppressor, but it has two basic characteristics of one, i.e. it is down-regulated in tumours and its expression is selectively cytotoxic to cancer cells. We have recently shown that ectopic expression of FDH in A549 lung cancer cells induces G1 arrest and apoptosis that was accompanied by elevation of p53 and its downstream target, p21. It was not known, however, whether FDH-induced apoptosis is p53-dependent or not. In the present study, we report that FDH-induced suppressor effects are strictly p53-dependent in A549 cells. Both knockdown of p53 using an RNAi (RNA interference) approach and disabling of p53 function by dominant-negative inhibition with R175H mutant p53 prevented FDH-induced cytotoxicity in these cells. Ablation of the FDH-suppressor effect is associated with an inability to activate apoptosis in the absence of functional p53. We have also shown that FDH elevation results in p53 phosphorylation at Ser-6 and Ser-20 in the p53 transactivation domain, and Ser-392 in the C-terminal domain, but only Ser-6 is strictly required to mediate FDH effects. Also, translocation of p53 to the nuclei and expression of the pro-apoptotic protein PUMA (Bcl2 binding component 3) was observed after induction of FDH expression. Elevation of FDH in p53 functional HCT116 cells induced strong growth inhibition, while growth of p53-deficient HCT116 cells was unaffected. This implies that activation of p53-dependent pathways is a general downstream mechanism in response to induction of FDH expression in p53 functional cancer cells.
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