ReviewFrontiers in bioscience (Landmark edition)2012
Proline metabolism and cancer.
Review in Frontiers in bioscience (Landmark edition), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 102 citations in OpenAlex.
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- Metabolomic Analysis of Intracellular Amino Acid Profile Differences Between Cisplatin-Resistant and Cisplatin- Sensitive CALU-1 Lung Cancer Cells.Cell biochemistry and biophysics · 2026Article
- CoQExperimental & molecular medicine · 2026Review
- Decoding amino acid metabolism in hepatocellular carcinoma: critical nodes and novel therapeutic strategy.Frontiers in oncology · 2026Review
- Glucagon and Glucose Availability Influence Metabolic Heterogeneity and Malignancy in Pancreatic Neuroendocrine Tumour (pNET) Cells: Novel Routes for Therapeutic Targeting.Molecules (Basel, Switzerland) · 2025Article
- ALDH4A1 functions as an active component of the MPC complex maintaining mitochondrial pyruvate import for TCA cycle entry and tumour suppression.Nature cell biology · 2025Article
- The new insight into the role of hydroxyproline in metabolism of cancer cells.Frontiers in cell and developmental biology · 2025Review
- Crystallographic Fragment Screening of a Bifunctional Proline Catabolic Enzyme Reveals New Inhibitor Templates for Proline Dehydrogenase and L-Glutamate-γ-semialdehyde Dehydrogenase.Molecules (Basel, Switzerland) · 2024Article
- Proline, a unique amino acid whose polymer, polyproline II helix, and its analogues are involved in many biological processes: a review.Amino acids · 2024Review
- Proline Metabolism in WHO G4 Gliomas Is Altered as Compared to Unaffected Brain Tissue.Cancers · 2024Article
- Monitoring Metabolic Changes in Response to Chemotherapies in Cancer with Raman Spectroscopy and Metabolomics.Analytical chemistry · 2023Article
- Amino acid metabolic reprogramming in tumor metastatic colonization.Frontiers in oncology · 2023Review
- Elevated Circulatory Proline to Glutamine Ratio (PQR) in Endometriosis and Its Potential as a Diagnostic Biomarker.ACS omega · 2022Article
- Review
- NSAIDs Induce Proline Dehydrogenase/Proline Oxidase-Dependent and Independent Apoptosis in MCF7 Breast Cancer Cells.International journal of molecular sciences · 2022Article
- Proline Dehydrogenase/Proline Oxidase (PRODH/POX) Is Involved in the Mechanism of Metformin-Induced Apoptosis in C32 Melanoma Cell Line.International journal of molecular sciences · 2022Article
- Structure-based engineering of minimal proline dehydrogenase domains for inhibitor discovery.Protein engineering, design & selection : PEDS · 2022Article
- Article
- Metformin Induces PRODH/POX-Dependent Apoptosis in Breast Cancer Cells.Frontiers in molecular biosciences · 2022Article
- Perspectives, past, present and future: the proline cycle/proline-collagen regulatory axis.Amino acids · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Proline plays a special role in cancer metabolism. Proline oxidase (POX), a.k.a. proline dehydrogenase (PRODH), is among a few genes induced rapidly and robustly by P53, the tumor suppressor. Ectopic expression of POX under control of tet-off promoter initiated mitochondrial apoptosis. The mechanism activated by POX is mediated by its production of ROS. In immunodeficient mice, POX overexpression markedly retarded growth of xenograft tumors. In human tumors of the digestive tract and kidney, POX was markedly decreased, suggesting that the suppressive effect of POX was downregulated. This was not due to POX gene mutations or hypermethylation. Instead, a microRNA, miR-23b*, expressed at high levels in tumors, was a potent inhibitor of POX expression. Furthermore, antagomirs of miR-23b* reversed the downregulated expression of POX and its tumor-suppressive effect, thereby providing a therapeutic strategy. POX not only responds to genotoxic stress, but also to inflammatory and metabolic stress. Depending on microenvironmental and temporal factors, POX can mediate oppositely-directed responses-programmed cell death, on the one hand, and survival, on the other.
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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.