ArticleJournal of translational medicine2017
A novel small molecule inhibitor of p32 mitochondrial protein overexpressed in glioma.
Article in Journal of translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- Circulating Metabolites Treat Human TMJ-OA by Eliminating Senescent Chondrocytes via the C1QBP/C1q/p14ARF Axis.Journal of extracellular vesicles · 2026Trial
- Unveiling the mysteries of C1QBP in gynecological tumors (Review).Molecular and clinical oncology · 2026Review
- Spatial multiomics profiling reveals ZFP36-mediated immunometabolic reprogramming in bladder cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Integrative pan-cancer genomic analysis highlights mitochondrial protein p32 as a potential therapeutic target in Myc-driven tumorigenesis.Medical oncology (Northwood, London, England) · 2025Article
- A new peptide inhibitor of C1QBP exhibits potent anti-tumour activity against triple negative breast cancer by impairing mitochondrial function and suppressing homologous recombination repair.Clinical and translational medicine · 2025Article
- Review
- Inhibition of Multifunctional Protein p32/C1QBP Promotes Cytostatic Effects in Colon Cancer Cells by Altering Mitogenic Signaling Pathways and Promoting Mitochondrial Damage.International journal of molecular sciences · 2024Article
- In silico identification and biological evaluation of a selective MAP4K4 inhibitor against pancreatic cancer.Journal of enzyme inhibition and medicinal chemistry · 2023Article
- C1QBP Mediates Breast Cancer Cell Proliferation and Growth via Multiple Potential Signalling Pathways.International journal of molecular sciences · 2023Article
- gC1qR: A New Target for Cancer Immunotherapy.Frontiers in immunology · 2023Review
- Role of gC1qR as a modulator of endothelial cell permeability and contributor to post-stroke inflammation and edema formation.Frontiers in cellular neuroscience · 2023Review
- Metabolic Labeling-Based Chemoproteomics Establishes Choline Metabolites as Protein Function Modulators.ACS chemical biology · 2022Article
- An approach to p32/gC1qR/HABP1: a multifunctional protein with an essential role in cancer.Journal of cancer research and clinical oncology · 2022Review
- C1QBP regulates mitochondrial plasticity to impact tumor progression and antitumor immune response.Frontiers in physiology · 2022Review
- p32 promotes melanoma progression and metastasis by targeting EMT markers, Akt/PKB pathway, and tumor microenvironment.Cell death & disease · 2021Article
- P32-specific CAR T cells with dual antitumor and antiangiogenic therapeutic potential in gliomas.Nature communications · 2021Article
- Overexpression of Multifunctional Protein p32 Promotes a Malignant Phenotype in Colorectal Cancer Cells.Frontiers in oncology · 2021Article
- Recent progress in LyP-1-based strategies for targeted imaging and therapy.Drug delivery · 2019Review
- Systematic Multiomics Analysis of Alterations in C1QBP mRNA Expression and Relevance for Clinical Outcomes in Cancers.Journal of clinical medicine · 2019Article
- Complement component 1q subcomponent binding protein in the brain of the rat.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe mitochondrial protein p32 is a validated therapeutic target of cancer overexpressed in glioma. Therapeutic targeting of p32 with monoclonal antibody or p32-binding LyP-1 tumor-homing peptide can limit tumor growth. However, these agents do not specifically target mitochondrial-localized p32 and would not readily cross the blood-brain barrier to target p32-overexpressing gliomas. Identifying small molecule inhibitors of p32 overexpressed in cancer is a more rational therapeutic strategy. Thus, in this study we employed a pharmacophore modeling strategy to identify small molecules that could bind and inhibit mitochondrial p32.
methodsA pharmacophore model of C1q and LyP-1 peptide association with p32 was used to screen a virtual compound library. A primary screening assay for inhibitors of p32 was developed to identify compounds that could rescue p32-dependent glutamine-addicted glioma cells from glutamine withdrawal. Inhibitors from this screen were analyzed for direct binding to p32 by fluorescence polarization assay and protein thermal shift. Affect of the p32 inhibitor on glioma cell proliferation was assessed by Alamar Blue assay, and affect on metabolism was examined by measuring lactate secretion.
resultsIdentification of a hit compound (M36) validates the pharmacophore model. M36 binds directly to p32 and inhibits LyP-1 tumor homing peptide association with p32 in vitro. M36 effectively inhibits the growth of p32 overexpressing glioma cells, and sensitizes the cells to glucose depletion.
conclusionsThis study demonstrates a novel screening strategy to identify potential inhibitors of mitochondrial p32 protein overexpressed in glioma. High throughput screening employing this strategy has potential to identify highly selective, potent, brain-penetrant small molecules amenable for further drug development.
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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.