ArticleCancer research2009
Proline oxidase functions as a mitochondrial tumor suppressor in human cancers.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
76 citing papers in PubMed, 125 citations in OpenAlex.
- Identification of a candidate PRODH allosteric inhibitor MBTP-15324: modulation of proline metabolite profiles and ECM-associated gene-expression changes in lung cancer cells.Journal of enzyme inhibition and medicinal chemistry · 2026Article
- Superoxide signals for the mitophagy of dysfunctional mitochondria to maintain quality control.Redox biology · 2026Review
- Serum Metabolomic Profiles Predict Sensitivity and Toxicity to Platinum- Fluorouracil Chemotherapy in a Gastric Cancer Xenograft Model.Combinatorial chemistry & high throughput screening · 2026Article
- Proline Metabolism in Cancer: Emerging Roles in Redox Homeostasis and Therapeutic Opportunities.Cancers · 2025Review
- Graphene Nanocomposites in the Targeting Tumor Microenvironment: Recent Advances in TME Reprogramming.International journal of molecular sciences · 2025Review
- Proline Metabolism in WHO G4 Gliomas Is Altered as Compared to Unaffected Brain Tissue.Cancers · 2024Article
- Proline Dehydrogenase (PRODH) Is Expressed in Lung Adenocarcinoma and Modulates Cell Survival and 3D Growth by Inducing Cellular Senescence.International journal of molecular sciences · 2024Article
- Loss of attachment promotes proline accumulation and excretion in cancer cells.Science advances · 2023Article
- Can proline dehydrogenase-a key enzyme involved in proline metabolism-be a novel target for cancer therapy?Frontiers in oncology · 2023Review
- Prolidase-proline oxidase axis is engaged in apoptosis induction by birch buds flavonol santin in endometrial adenocarcinoma cell line.Frontiers in molecular biosciences · 2023Article
- Proline Metabolism in Neurological and Psychiatric Disorders.Molecules and cells · 2022Review
- Review
- NSAIDs Induce Proline Dehydrogenase/Proline Oxidase-Dependent and Independent Apoptosis in MCF7 Breast Cancer Cells.International journal of molecular sciences · 2022Article
- Understanding the Role of Estrogen Receptor Status in PRODH/POX-Dependent Apoptosis/Survival in Breast Cancer Cells.Biology · 2021Review
- Perspectives, past, present and future: the proline cycle/proline-collagen regulatory axis.Amino acids · 2021Article
- Proline metabolism in cancer.Amino acids · 2021Review
- Review
- Proline dehydrogenase in cancer: apoptosis, autophagy, nutrient dependency and cancer therapy.Amino acids · 2021Review
- Proline oxidase silencing inhibits p53-dependent apoptosis in MCF-7 breast cancer cells.Amino acids · 2021Article
- Collagen metabolism as a regulator of proline dehydrogenase/proline oxidase-dependent apoptosis/autophagy.Amino acids · 2021Review
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Tumor metabolism and bioenergetics have become important topics for cancer research and are promising targets for anticancer therapy. Although glucose serves as the main source of energy, proline, an alternative substrate, is important, especially during nutrient stress. Proline oxidase (POX), catalyzing the first step in proline catabolism, is induced by p53 and can regulate cell survival as well as mediate programmed cell death. In a mouse xenograft tumor model, we found that POX greatly reduced tumor formation by causing G2 cell cycle arrest. Furthermore, immunohistochemical staining showed decreased POX expression in tumor tissues. Importantly, HIF-1alpha signaling was impaired with POX expression due to the increased production of alpha-ketoglutarate, a critical substrate for prolyl hydroxylation and degradation of HIF-1alpha. Combined with previous in vitro findings and reported clinical genetic associations, these new findings lead us to propose POX as a mitochondrial tumor suppressor and a potential target for cancer therapy.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.