ArticleCancers2024
Spatial Genomics Identifies Heat Shock Proteins as Key Molecular Changes Associated to Adipose Periprostatic Space Invasion in Prostate Cancer.
Article in Cancers, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- SARIFA and Lipid Metabolic Reprogramming in Prostate Cancer: Fundamental Mechanisms, Tumor Microenvironment, and Novel Biomarker Prospects.Life (Basel, Switzerland) · 2026Review
- Unraveling the carcinogenic mechanisms of benzo[a]pyrene in prostate cancer: a multi-omics approach.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Advancing prostate cancer research: an exploration of periprostatic adipose stem cells.Journal of translational medicine · 2025Review
- Cysteine Alkylation in Enzymes and Transcription Factors: A Therapeutic Strategy for Cancer.Cancers · 2025Review
- Mendelian randomization analysis reveals potential causal relationships between serum lipid metabolites and prostate cancer risk.Discover oncology · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
purposeTo identify molecular changes during PCa invasion of adipose space using Spatial Transcriptomic Profiling of PCa cells.
methodsThis study was performed on paired intraprostatic and extraprostatic samples obtained from radical prostatectomy with pT3a pathological stages.
resultsDifferential gene expression revealed upregulation of heat shock protein genes: DNAJB1, HSPA8, HSP90AA1, HSPA1B, HSPA1A in PCa PanCK+ cells from the adipose periprostatic space. Extraprostatic extension was significantly associated with overexpression of genes involved in metastatic spread (EGR1, OR51E2, SPON2), of aggressiveness ERG negative signature of enhancers of androgen receptor (HOXB13, FOXA1), and of PSMA (FOLH1). They were associated with loss at 6q, 10q, 16q, and gain at 8q24 locus.
conclusionsPCa invasion of adipose EPE induces adaptative process related to heat shock proteins; PCa cells in EPE also present transcriptomics signatures for ERG independent aggressiveness, androgen receptor co-activation, and specific CNV changes.
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