ArticleOncotarget2015
Anti-cancer efficacy of SREBP inhibitor, alone or in combination with docetaxel, in prostate cancer harboring p53 mutations.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 74 citations in OpenAlex.
- Reprogrammed Lipid Metabolism-Associated Therapeutic Vulnerabilities in Prostate Cancer.International journal of molecular sciences · 2025Review
- Review
- Tumor innervation and mitochondrial transfer in the cancer pathogenesis: perspectives on genitourinary malignancies.Frontiers in oncology · 2025Review
- SREBP2 as a central player in cancer progression: potential for targeted therapeutics.Frontiers in pharmacology · 2025Review
- From regulation to deregulation of p53 in hematologic malignancies: implications for diagnosis, prognosis and therapy.Biomarker research · 2024Review
- Inhibition of the Sterol Regulatory Element Binding Protein SREBF-1 Overcomes Docetaxel Resistance in Advanced Prostate Cancer.The American journal of pathology · 2024Article
- Cholesterol Metabolism and Urinary System Tumors.Biomedicines · 2024Review
- The SARIFA biomarker in the context of basic research of lipid-driven cancers.NPJ precision oncology · 2024Review
- Cholesterol metabolism in tumor microenvironment: cancer hallmarks and therapeutic opportunities.International journal of biological sciences · 2024Review
- Unraveling the intricate relationship between lipid metabolism and oncogenic signaling pathways.Frontiers in cell and developmental biology · 2024Review
- Differential Proteome Profiling Analysis under Pesticide Stress by the Use of a Nano-UHPLC-MS/MS Untargeted Proteomic-Based Approach on a 3D-Developed Neurospheroid Model: Identification of Protein Interactions, Prognostic Biomarkers, and Potential Therapeutic Targets in Human IDH Mutant High-Grade Gliomas.Journal of proteome research · 2023Article
- Lipid metabolic reprogramming in tumor microenvironment: from mechanisms to therapeutics.Journal of hematology & oncology · 2023Review
- Regulatory Role of Fatty Acid Metabolism-Related Long Noncoding RNA in Prostate Cancer: A Computational Biology Study Analysis.Journal of oncology · 2023Article
- The role of cholesterol metabolism in tumor therapy, from bench to bed.Frontiers in pharmacology · 2023Review
- Key events in cancer: Dysregulation of SREBPs.Frontiers in pharmacology · 2023Review
- Targeting lipid metabolism in metastatic prostate cancer.Therapeutic advances in medical oncology · 2023Review
- The Aurora Kinase Inhibitor TAK901 Inhibits Glioblastoma Growth by Blocking SREBP1-Mediated Lipid Metabolism.Cancers · 2022Article
- Role of Lipids and Lipid Metabolism in Prostate Cancer Progression and the Tumor's Immune Environment.Cancers · 2022Review
- Lipid Metabolism and Epigenetics Crosstalk in Prostate Cancer.Nutrients · 2022Review
- Lipid Droplets in Cancer: From Composition and Role to Imaging and Therapeutics.Molecules (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mutant p53 proteins (mutant p53s) have oncogenic gain-of-function properties correlated with tumor grade, castration resistance, and prostate cancer (PCa) tumor recurrence. Docetaxel is a standard first-line treatment for metastatic castration-resistant PCa (mCRPC) after the failure of hormone therapy. However, most mCRPC patients who receive docetaxel experience only transient benefits and rapidly develop incurable drug resistance, which is closely correlated with the p53 mutation status. Mutant p53s were recently reported to regulate the metabolic pathways via sterol regulatory element-binding proteins (SREBPs). Therefore, targeting the SREBP metabolic pathways with docetaxel as a combination therapy may offer a potential strategy to improve anti-tumor efficacy and delay cellular drug resistance in mCRPC harboring mutant p53s. Our previous data showed that fatostatin, a new SREBP inhibitor, inhibited cell proliferation and induced apoptosis in androgen receptor (AR)-positive PCa cell lines and xenograft mouse models. In this study, we demonstrated that mutant p53s activate the SREBP-mediated metabolic pathways in metastatic AR-negative PCa cells carrying mutant p53s. By blocking the SREBP pathways, fatostatin inhibited cell growth and induced apoptosis in metastatic AR-negative PCa cells harboring mutant p53s. Furthermore, the combination of fatostatin and docetaxel resulted in greater proliferation inhibition and apoptosis induction compared with single agent treatment in PCa cells in vitro and in vivo, especially those with mutant p53s. These data suggest for the first time that fatostatin alone or in combination with docetaxel could be exploited as a novel and promising therapy for metastatic PCa harboring p53 mutations.
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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.