ArticleMolecular cancer research : MCR2023
Subtype and Site Specific-Induced Metabolic Vulnerabilities in Prostate Cancer.
Article in Molecular cancer research : MCR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Metabolism in Tumour-Induced Bone Disease.Current osteoporosis reports · 2026Review
- Adverse prognosis gene expression patterns in metastatic castration-resistant prostate cancer.Molecular oncology · 2025Article
- Cell-intrinsic metabolic phenotypes identified in patients with glioblastoma, using mass spectrometry imaging ofNature metabolism · 2025Article
- Metabolic imaging distinguishes ovarian cancer subtypes and detects their early and variable responses to treatment.Oncogene · 2025Article
- Mitochondrial involvement in PC: improving therapeutic strategies.Frontiers in pharmacology · 2025Review
- Therapeutic modulation of ROCK overcomes metabolic adaptation of cancer cells to OXPHOS inhibition and drives synergistic anti-tumor activity.bioRxiv : the preprint server for biology · 2024Article
- Deuterium Metabolic Imaging Differentiates Glioblastoma Metabolic Subtypes and Detects Early Response to Chemoradiotherapy.Cancer research · 2024Article
- Imaging cancer metabolism using magnetic resonance.Npj imaging · 2024Review
- MYC is a regulator of androgen receptor inhibition-induced metabolic requirements in prostate cancer.Cell reports · 2023Article
- Aggressive variant prostate cancer: A case report and literature review.World journal of clinical cases · 2023Article
- Editorial: Complexity of tumor microenvironment: A major culprit in cancer development.Frontiers in endocrinology · 2022Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
Aberrant metabolic functions play a crucial role in prostate cancer progression and lethality. Currently, limited knowledge is available on subtype-specific metabolic features and their implications for treatment. We therefore investigated the metabolic determinants of the two major subtypes of castration-resistant prostate cancer [androgen receptor-expressing prostate cancer (ARPC) and aggressive variant prostate cancer (AVPC)]. Transcriptomic analyses revealed enrichment of gene sets involved in oxidative phosphorylation (OXPHOS) in ARPC tumor samples compared with AVPC. Unbiased screening of metabolic signaling pathways in patient-derived xenograft models by proteomic analyses further supported an enrichment of OXPHOS in ARPC compared with AVPC, and a skewing toward glycolysis by AVPC. In vitro, ARPC C4-2B cells depended on aerobic respiration, while AVPC PC3 cells relied more heavily on glycolysis, as further confirmed by pharmacologic interference using IACS-10759, a clinical-grade inhibitor of OXPHOS. In vivo studies confirmed IACS-10759's inhibitory effects in subcutaneous and bone-localized C4-2B tumors, and no effect in subcutaneous PC3 tumors. Unexpectedly, IACS-10759 inhibited PC3 tumor growth in bone, indicating microenvironment-induced metabolic reprogramming. These results suggest that castration-resistant ARPC and AVPC exhibit different metabolic dependencies, which can further undergo metabolic reprogramming in bone. IMPLICATIONS: These vulnerabilities may be exploited with mechanistically novel treatments, such as those targeting OXPHOS alone or possibly in combination with existing therapies. In addition, our findings underscore the impact of the tumor microenvironment in reprogramming prostate cancer metabolism.
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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 Socratic graph.