ArticleGenes & cancer2019
Inactivated FABP5 suppresses malignant progression of prostate cancer cells by inhibiting the activation of nuclear fatty acid receptor PPARγ.
Article in Genes & cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- Targeting the Fatty Acid Binding Protein 5-Specificity Protein 1 Axis Restores Enzalutamide Sensitivity by Suppressing Androgen Receptor/Androgen Receptor Splice Variant 7 Signaling: Implications for Prostate Cancer Therapy.World journal of oncology · 2026Article
- Microenvironmentally derived fatty acid-binding proteins 4 and 5 are novel therapeutic vulnerabilities in multiple myeloma.Blood neoplasia · 2026Article
- SBFI Inhibitors Reprogram Transcriptomic Landscape of Prostate Cancer Cells Leading to Cell Death.Cancers · 2025Article
- Reprogrammed Lipid Metabolism-Associated Therapeutic Vulnerabilities in Prostate Cancer.International journal of molecular sciences · 2025Review
- Dual function of activated PPARγ by ligands on tumor growth and immunotherapy.Medical oncology (Northwood, London, England) · 2024Review
- FABP5 can substitute for androgen receptor in malignant progression of prostate cancer cells.International journal of oncology · 2024Article
- Unraveling the intricate relationship between lipid metabolism and oncogenic signaling pathways.Frontiers in cell and developmental biology · 2024Review
- Experimental treatment efficacy of dmrFABP5 on prostate cancer singly or in combination with drugs in use.American journal of cancer research · 2024Article
- FABP5 Inhibition againstCancers · 2023Article
- Multiomic analysis of cervical squamous cell carcinoma identifies cellular ecosystems with biological and clinical relevance.Nature genetics · 2023Article
- FABP5 regulates lipid metabolism to facilitate pancreatic neuroendocrine neoplasms progression via FASN mediated Wnt/β-catenin pathway.Cancer science · 2023Article
- Fatty acid binding protein 5 regulates docetaxel sensitivity in taxane-resistant prostate cancer cells.PloS one · 2023Article
- Interplay between Prostate Cancer and Adipose Microenvironment: A Complex and Flexible Scenario.International journal of molecular sciences · 2022Review
- How cancer cells remodel lipid metabolism: strategies targeting transcription factors.Lipids in health and disease · 2021Review
- An Amplified Fatty Acid-Binding Protein Gene Cluster in Prostate Cancer: Emerging Roles in Lipid Metabolism and Metastasis.Cancers · 2020Review
- Crystal Engineering Construction of Caffeic Acid Derivatives with Potential Applications in Pharmaceuticals and Degradable Polymeric Materials.CrystEngComm · 2020Article
- The FABP12/PPARγ pathway promotes metastatic transformation by inducing epithelial-to-mesenchymal transition and lipid-derived energy production in prostate cancer cells.Molecular oncology · 2020Article
- FABP5 as a novel molecular target in prostate cancer.Drug discovery today · 2020Review
- Important players in carcinogenesis as potential targets in cancer therapy: an update.Oncotarget · 2020Review
- Fatty acid-binding protein 5 (FABP5)-related signal transduction pathway in castration-resistant prostate cancer cells: a potential therapeutic target.Precision clinical medicine · 2019Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
Abstract
Previous study has suggested that the FABP5-PPARγ-signalling transduction pathway gradually replaces the androgen receptor activated pathway in promoting malignant progression of castration-resistant prostate cancer (CRPC) cells. To interfere with this newly discovered FABP5-related signalling pathway, we have produced a highly efficient recombinant FABP5 inhibitor, named dmrFABP5. Treatment with dmrFABP5 significantly supressed the proliferation, migration, invasion and colony formation of the highly malignant prostate cancer cells PC3-M
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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.