bims-meproc Biomed News
on Metabolism in Prostate Cancer
Issue of 2025–09–28
25 papers selected by
Grigor Varuzhanyan, UCLA



  1. Int J Mol Sci. 2025 Sep 18. pii: 9132. [Epub ahead of print]26(18):
      Prostate cancer (PCa), the second leading cause of cancer-related mortality among men in the United States, is marked by profound metabolic reprogramming, particularly in lipid metabolism. This review highlights the pivotal role of altered lipid metabolic pathways, including de novo fatty acid synthesis, fatty acid uptake and transport, β-oxidation, and cholesterol metabolism, in the development, progression, and therapeutic resistance of PCa. Key enzymes and transcription factors, such as FASN, ACLY, SREBPs, and FABPs, which are mainly regulated by androgen receptor signaling, orchestrate a lipogenic phenotype that supports prostate tumor growth and survival. Crosstalk between lipid metabolism and the tumor microenvironment further promotes immune evasion and metastasis. The review also explores therapeutic opportunities in targeting lipid metabolic pathways, highlighting the preclinical and clinical advances in inhibiting FASN, SREBP1, SREBP2, HMGCR, and FABPs, as well as combinatorial strategies with conventional therapies. Understanding the impact of lipid metabolism on PCa pathogenesis provides a promising avenue for developing novel targeted and combinatorial interventions to improve clinical outcomes in PCa.
    Keywords:  cholesterol metabolism; fatty acid metabolism; lipid metabolism; prostate cancer; prostate cancer therapy
    DOI:  https://doi.org/10.3390/ijms26189132
  2. J Pharmacol Exp Ther. 2025 Aug 28. pii: S0022-3565(25)39897-6. [Epub ahead of print]392(10): 103684
      Neuroendocrine prostate cancer (NEPC) is a highly aggressive subtype of prostate cancer with poor prognosis and limited therapeutic options. Targeting cancer metabolism is a promising strategy for treating NEPC. This study investigated the antitumor activity and underlying mechanisms of koningic acid (KA), a selective glyceraldehyde-3-phosphate dehydrogenase inhibitor, in NEPC. NEPC cell models (PC3, LNCaP-NE, and NCI-H660) were treated with KA to assess its effects on cell viability, colony formation, glycolysis, mitochondrial function, and apoptosis. Xenograft models were used to evaluate in vivo tumor growth. Key markers and pathways were analyzed using quantitative polymerase chain reaction, western blotting, and immunohistochemistry. In this study, KA significantly inhibited cell proliferation and colony formation, with IC50 values of 5.73 μM in PC3, 7.57 μM in LNCaP-NE, and 6.32 μM in NCI-H660 cells. Glycolysis was markedly suppressed, as indicated by reduced extracellular acidification rate, lactate production, and glucose uptake. KA also induced mitochondrial dysfunction, evidenced by decreased mitochondrial membrane potential, increased reactive oxygen species, and reduced ATP levels. Furthermore, KA decreased phospho (p)-Akt and p-glycogen synthase kinase-3β expression, leading to apoptosis activation. In xenograft models, KA treatment reduced tumor size, weight, and expression of Ki67, p-Akt, and of lactate dehydrogenase A, while increasing levels of apoptosis markers. In conclusion, KA exerts significant antitumor effects in NEPC by inhibiting glycolysis and inducing mitochondrial apoptosis. These findings highlight its potential as a therapeutic agent for NEPC. SIGNIFICANCE STATEMENT: Koningic acid (KA) inhibits glycolysis and suppresses proliferation in neuroendocrine prostate cancer cells by targeting glyceraldehyde-3-phosphate dehydrogenase. KA induces mitochondrial dysfunction, increases reactive oxygen species production, and activates apoptosis through downregulation of phospho-Akt and phospho-glycogen synthase kinase-3β signaling. In vivo studies demonstrate that KA reduces tumor growth and proliferation while promoting apoptosis, highlighting its potential as a therapeutic agent for neuroendocrine prostate cancer.
    Keywords:  Glycolysis; Koningic acid; Mitochondrial apoptosis; Neuroendocrine prostate cancer
    DOI:  https://doi.org/10.1016/j.jpet.2025.103684
  3. Adv Biol (Weinh). 2025 Sep 24. e00182
      Small nucleolar RNAs (snoRNAs)-60-300 nucleotide non-coding RNAs are associated with adverse clinical outcomes in cancer patients. However, information on the role of snoRNAs and associated small nuclear ribonucleoprotein (snoRNPs) in prostate cancer (PCa) remains scarce. Here, the contribution of the snoRNP U3 snoRNA-interacting protein 2 (RRP9) in PCa pathogenesis is investigated. A combination of three different shRNAs is employed to knockdown RRP9 in the PCa cell lines DU-145 and PC-3. Cell proliferation is evaluated by seeding cells into a 96-well plates and monitoring daily. Cell migration is evaluated by scratch and Transwell assays. FLAG-RRP9 pull-down, MALDI-TOF/TOF, and co-immunoprecipitation assays are conducted to identify RRP9 binding partners in DU-145 cells. In vitro cell proliferation and migration, as well as in vivo tumor growth, are suppressed following RRP9 knockdown. Pull-down and MALDI-TOF/TOF analyses identified five putative RRP9 binding partners, and co-immunoprecipitation validated that RRP9 interacts with the scaffolding hub protein Sequestome-1 (SQSTM1, p62). Interestingly, SQSTM1 overexpression rescued the anti-growth/migration effects of RRP9 knockdown. This study unveiled a novel oncogenic role for the RRP9-SQSTM1 axis in PCa cells. RRP9 is a snoRNP that binds to SQSTM1, thereby promoting PCa cell proliferation and migration. Targeting the RRP9-SQSTM1 axis may be a viable therapeutic strategy for PCa.
    Keywords:  RRP9; SQSTM1; p62; prostate cancer; snoRNP
    DOI:  https://doi.org/10.1002/adbi.202500182
  4. Biochem Biophys Res Commun. 2025 Sep 16. pii: S0006-291X(25)01362-2. [Epub ahead of print]784 152646
      Prostate cancer (PCa) is the most prevalent male malignancies globally, and its incidence and mortality rates are constantly rising. The current study focuses on the novel molecular mechanism affecting PCa progression. Through analyzing the GSE246282 dataset, OR51F2 was selected as the research target because it presented the most significantly upregulation in PCa tissues. Moreover, OR51F2 expression was detected and found to be high in PCa cells at both mRNA and protein levels. Functionally, PCa cell proliferation and migration were repressed efficiently by silencing of OR51F2 expression. Mechanistically, OR51F2 protein was stabilized by OGT-induced O-GlcNAcylation. Furthermore, OGT overexpression led to the recovery of OGT silencing-induced suppression of PCa cell proliferation and migration. Dysregulation of signaling pathways contributes to tumorigenesis and cancer progression. Here, we determined that OGT and OR51F2 could activate Wnt/β-catenin signaling pathway. Finally, activation of Wnt pathway by LiCl treatment recovered the proliferation and migration of PCa cells repressed by OGT silencing. In conclusion, the present study indicated that OGT-induced O-GlcNAcylation of OR51F2 accelerated PCa progression via activating the Wnt/β-catenin pathway.
    Keywords:  O-GlcNAcylation; OGT; OR51F2; Prostate cancer; Wnt/β-catenin pathway
    DOI:  https://doi.org/10.1016/j.bbrc.2025.152646
  5. Antioxidants (Basel). 2025 Aug 28. pii: 1060. [Epub ahead of print]14(9):
      Prostate cancer is not only the most common type of cancer in elderly American men but also the 2nd leading cause of cancer death in American men. The currently available treatments in clinics target male hormones that are majorly required for maintaining many physiological functions, including muscle strength, leading to poor life quality and subsequent patient-opted intermittent treatment. Aging is a key factor in prostate cancer that is associated with increased levels of oxidative stress. Several lines of evidence indicated elevated levels of reactive oxygen species (ROS) in prostate cancer, including its precursor, prostate intraepithelial neoplasia (PIN). In this current study, we utilized 4-hydroxynonenal (4HNE) as a general readout for overall oxidative stress to demonstrate the imbalance between ROS and antioxidants in human prostate cancer and its precursor lesion in both human culture cell lines and tissue samples. Our results showed that the production of 4HNE adducts was increased in human prostate cancer cells and was non-linearly correlated with prostate cancer stage. They also provided insight into prevention and potential therapeutic strategies for prostate cancer.
    Keywords:  4HNE protein adducts; inflammation; oxidative stress; prostate cancer; prostate intraepithelial neoplasia; reactive oxygen species
    DOI:  https://doi.org/10.3390/antiox14091060
  6. Antioxidants (Basel). 2025 Sep 15. pii: 1120. [Epub ahead of print]14(9):
      Glyoxalase 1 (Glo1) functions as a catalyst that neutralizes methylglyoxal (MG), a highly reactive glycating agent predominantly produced during glycolysis-a metabolic pathway upregulated in cancer cells. MG primarily reacts with the amino groups of proteins (especially at arginine residues), leading to the formation of a major advanced glycation end product known as MG-derived hydroimidazolone 1 (MG-H1). We previously demonstrated in PC3 human prostate cancer (PCa) cells that the PTEN/PKM2/ERα axis promotes their aggressive phenotype by regulating the Glo1/MG-H1 pathway. In this study, after confirming our earlier findings, we investigated the downstream mechanisms of the PTEN/PKM2/ERα/Glo1/MG-H1 axis in controlling PC3 cell growth, focusing on the role of RAGE, a high-affinity receptor for MG-H1; hydrogen peroxide (H2O2); and Krev interaction trapped 1 (KRIT1), an emerging tumor suppressor. Using genetic approaches and specific inhibitors/scavengers, we demonstrated that the PTEN/PKM2/ERα/Glo1/MG-H1 axis promotes PC3 cell growth-measured by proliferation and etoposide-induced apoptosis resistance-through a mechanism involving MG-H1/RAGE pathway desensitization that leads to H2O2-mediated KRIT1 downregulation. These findings support and expand the role of PTEN signaling in PCa progression and shed light on novel mechanistic pathways driven by MG-dependent glycative stress, involving KRIT1, in this still incurable stage of the disease.
    Keywords:  H2O2; KRIT1; MG-H1; PC3; PTEN; RAGE; glyoxalase 1; prostate cancer
    DOI:  https://doi.org/10.3390/antiox14091120
  7. Int J Mol Sci. 2025 Sep 15. pii: 8991. [Epub ahead of print]26(18):
      Cysteine-rich angiogenic inducer 61 (CYR61) promotes prostate cancer (PCa) cell growth, but its role in disease progression remains unclear. Given its insulin-like growth factor (IGF)-binding domain and the known involvement of insulin-like growth factor-1 (IGF1) in PCa, we investigated the molecular interplay between CYR61 and IGF1. CYR61 was silenced using small interfering RNA (siRNA) in prostate carcinoma 3 (PC3), lymph node carcinoma of the prostate (LNCaP), and androgen receptor (AR)-positive 22Rv1 cells, followed by assessments of their proliferation, viability, colony formation, migration, and signaling pathway activation. CYR61 knockdown significantly reduced cell growth, viability, prostasphere formation, and migration across all three cell lines. Mechanistically, CYR61 silencing inhibited PI3K/AKT signaling but had no effect on MAPK activation. In addition, treatment with recombinant IGF1 induced CYR61 expression in a time-dependent manner, and the inhibition of PI3K/AKT signaling suppressed both CYR61 expression and cell proliferation. These findings suggest that IGF1 promotes PCa progression through CYR61 and that CYR61 may serve as a potential therapeutic target for limiting tumor growth and metastasis.
    Keywords:  CYR61; IGF1; MAPK; PI3/AKT; metabolism; metastasis; prostate cancer
    DOI:  https://doi.org/10.3390/ijms26188991
  8. Front Oncol. 2025 ;15 1630181
       Background: Prostate cancer is a common malignancy in men with limited effective treatment options, highlighting an urgent need for novel therapeutic approaches. Osthole, a natural coumarin compound with antitumor properties, has shown potential in targeting various cancers.
    Methods: We conducted the study using a combination of network pharmacology, in vitro assays, and in vivo experiments. First, network pharmacology was used to predict the potential targets of Osthole, identifying 68 targets shared with prostate cancer, including AKT1, TNF, IL6, STAT3, and CTNNB1. Subsequently, we confirmed these targets and assessed the effects of Osthole on cell proliferation, migration, and apoptosis using the Cell Counting Kit-8 (CCK-8) and transwell invasion assays. Meanwhile, molecular docking and western blot analysis were employed to analyze molecular interactions and protein expression levels.
    Results: Our findings revealed that Osthole significantly inhibited prostate cancer cell proliferation and migration in a dose-dependent manner and reduced tumor volume in in vivo assays. Western blot analysis indicated that Osthole downregulated PRLR expression and decreased the phosphorylation of JAK2 and STAT3, suggesting the inhibition of the JAK2/STAT3 signaling pathway.
    Conclusion: These results collectively highlight the therapeutic potential of Osthole in targeting prostate cancer cells through PRLR and modulating the JAK2/STAT3 signaling pathway, warranting further clinical exploration.
    Keywords:  JAK2/STAT3 pathway; PRLR; network pharmacology; osthole; prostate cancer
    DOI:  https://doi.org/10.3389/fonc.2025.1630181
  9. Prostate Cancer. 2025 ;2025 8862153
      Background: Fibroblast growth factor receptor 1 (FGFR1) signaling is activated by fibroblast growth factors (FGFs) during prostate cancer (PCa) progression. However, the mechanisms by which FGFR1 signaling regulates PCa progression are not fully understood. The objective of this study was to investigate the cross talk between autocrine FGF/FGFR1 loop and aerobic glycolysis in progression of advanced PCa. Method: DU145 cells were used as an advanced PCa model. FGFR1 expression was knockdowned by stable expression of anti-FGFR1 shRNA, and lactate dehydrogenase A (LDHA) levels were rescued by ectopic expression of LDHA cDNA. Protein expression was determined using Western blotting and immunohistochemistry. Tumorigenicity of DU145 cells was defined by cell growth, invasion, and survival in both cultures and xenografts in mice. Results: Here, we showed that DU145 cells in cultures expressed both FGF2 and FGFR1, and knockdown of FGFR1 expression or inactivation of FGFR1 signaling reduced LDHA expression or aerobic glycolysis, which was correlated with suppression of both cell proliferation and invasion, and with promotion of apoptosis. Ectopic expression of LDHA cDNA rescued LDHA levels in FGFR1-deficient cells, restoring their aerobic glycolysis, cell growth, and survival. Similarly, the growth rates of xenografted DU145 cells in mice were decreased by the loss of FGFR1 expression but were rescued by the ectopic expression of LDHA. Conclusion: Our data indicate autocrine FGF/FGFR1 signaling regulates aerobic glycolysis in PCa DU145 cells via LDHA, suggesting the potential of targeting FGFs/FGFRs-LDHA for the management of advanced PCa. The regulation of aerobic glycolysis by other growth factors in PCa remains further investigation.
    Keywords:  aerobic glycolysis; autocrine FGF/FGFR; prostate cancer; tumor development
    DOI:  https://doi.org/10.1155/proc/8862153
  10. Anticancer Res. 2025 Oct;45(10): 4381-4388
       BACKGROUND/AIM: Lineage plasticity enables prostate cancer cells to bypass androgen receptor (AR) dependence, contributing to metastasis, treatment resistance, and lethality. The developmental transcription factor PROX1 was recently identified as an early driver of lineage plasticity. The TMPRSS2-ERG fusion, a common genomic event in prostate cancer, induces ERG overexpression and aggressive tumor behavior. We investigated the relationship between PROX1 expression and ERG expression in the context of TMPRSS2-ERG fusion in prostate cancer.
    MATERIALS AND METHODS: We analyzed data from The Cancer Genome Atlas (TCGA) Prostate Adenocarcinoma (PRAD) dataset (n=492 samples). The UCSC Xena Browser was used to visualize and integrate gene expression, copy number alterations, and fusion status. Complementary analyses were performed using cBioPortal. Genomic instability was assessed using both fraction of the genome altered (FGA) and mutation count. The correlation between PROX1 and ERG expression was evaluated in fusion-positive and fusion-negative tumors.
    RESULTS: PROX1 expression showed a strong positive correlation with ERG expression in TMPRSS2-ERG fusion-positive tumors (r=0.4, p=3.2×10-16). Fusion-positive samples exhibited elevated PROX1 expression, compared to fusion-negative samples. This pattern suggests that PROX1 induction is associated with ERG-driven transcriptional reprogramming linked to the TMPRSS2-ERG fusion.
    CONCLUSION: PROX1 expression is significantly associated with ERG expression and TMPRSS2-ERG fusion status in prostate cancer. These findings reinforce the role of PROX1 as an early marker and potential mediator of lineage plasticity. Targeting PROX1 or its regulatory pathways may offer a novel therapeutic strategy to mitigate plasticity-driven progression and treatment resistance in TMPRSS2-ERG fusion-positive prostate cancer.
    Keywords:  ERG oncogene; PROX1; Prostate cancer; TMPRSS2-ERG fusion; lineage plasticity
    DOI:  https://doi.org/10.21873/anticanres.17787
  11. Oncogene. 2025 Sep 23.
      PI3K-AKT signaling axis is often aberrantly activated in human cancers including prostate cancer, but the underlying mechanism of deregulation and tactics for effective targeting of this cancer relevant pathway remain poorly understood. Here, we demonstrate that KBTBD11 E3 ubiquitin ligase gene is frequently deleted in human prostate cancers and that KBTBD11 loss augments AKT phosphorylation in prostate cancer cells in culture and in patient samples. We show that KBTBD11 promotes lysine-27-chain polyubiquitination at lysine 8 and 14 on AKT and antagonizes ubiquitin K63 linkage-mediated polyubiquitination and phosphorylation of AKT. KBTBD11 deficiency drove prostate cancer cell growth in vitro and in vivo, but constituted as a therapeutic vulnerability to the selective AKT inhibitor in prostate cancer. Our study identifies lysine-27-chain polyubiquitination as an inhibitory mechanism of AKT activation and nominates KBTBD11 as an intrinsic upstream inhibitor of AKT. Our findings suggest that KBTBD11 deletion could be a biomarker to guide the use of the AKT inhibitors for the effective treatment of cancers such as prostate cancer.
    DOI:  https://doi.org/10.1038/s41388-025-03576-w
  12. Discov Oncol. 2025 Sep 26. 16(1): 1733
       BACKGROUND: Metabolic reprogramming and immune landscape remodeling are hallmarks of prostate cancer (PCa) progression and therapy resistance. However, the interplay between tumor metabolism, immune infiltration, and prognosis remains poorly characterized.
    METHODS: We obtained transcriptomic and clinical data of PCa patients from The Cancer Genome Atlas (TCGA). Single-sample gene set enrichment analysis (ssGSEA) was used to assess metabolic pathway activity and define metabolic subtypes. Immune infiltration was evaluated using multiple algorithms, including CIBERSORT and xCell. Prognostic genes were identified through univariate Cox and LASSO regression analyses, and a metabolic risk model was constructed and validated. Functional enrichment, immune checkpoint expression, and clinical associations were further analyzed. A nomogram was developed by integrating clinical features and risk scores.
    RESULTS: Two distinct metabolic subtypes-Metabolism_H and Metabolism_L-were identified, exhibiting differential metabolic activity, immune infiltration, and clinical outcomes. The Metabolism_H group showed upregulation of lipid and amino acid metabolism pathways and was associated with an immunosuppressive microenvironment and worse prognosis. A robust metabolic risk score derived from 14 prognostic genes significantly stratified patients by overall survival (p < 0.001). The risk score positively correlated with PD-L1 expression and immune exclusion features. The integrated nomogram demonstrated strong predictive power for 1-, 3-, and 5-year survival (AUC > 0.74) and good calibration.
    CONCLUSION: Our findings highlight the metabolic and immunological heterogeneity of prostate cancer and provide a novel metabolism-based prognostic model. Targeting tumor metabolism may enhance immune responses and improve risk stratification and therapeutic outcomes in PCa patients.
    Keywords:  Immune infiltration; LASSO; Metabolism; PD-L1; Prognostic model; Prostate cancer; TCGA; ssGSEA
    DOI:  https://doi.org/10.1007/s12672-025-03269-6
  13. FASEB J. 2025 Sep 30. 39(18): e71063
      Prostate cancer (PCa) is a common and aggressive malignancy in men, often diagnosed at advanced stages with a poor five-year survival rate. Despite therapeutic advances, effective treatments for castration-resistant PCa remain lacking. Timosaponin A3 (TA3), a natural steroidal saponin derived from Anemarrhena asphodeloides Bunge, has shown potential anti-tumor properties, but its role in PCa and the underlying mechanisms have not been fully elucidated. In this study, we demonstrate that TA3 significantly inhibits the proliferation, migration, and invasion of PCa cells in vitro, and suppresses tumor growth in xenograft models. Transcriptomic analysis revealed that TA3 exerts its anti-tumor effects by modulating cholesterol metabolism. Elevated cholesterol levels were observed in PCa patients, and exogenous cholesterol administration reduced tumor growth in vivo. Notably, TA3 treatment upregulated the lipid transporter StAR related lipid transfer domain containing 4 (STARD4), a key regulator of cholesterol transport, which was confirmed to mediate the inhibitory effects of TA3 on PCa progression. Overexpression of STARD4 attenuated PCa development both in vitro and in vivo, while STARD4 knockdown abolished these effects. Collectively, our findings suggest that TA3 suppresses PCa progression by enhancing cholesterol metabolism via STARD4 upregulation, supporting its potential as a novel therapeutic agent for prostate cancer.
    Keywords:  STARD4; cholesterol metabolism; metastasis; proliferation; prostate cancer; timosaponin A3
    DOI:  https://doi.org/10.1096/fj.202501885R
  14. Cell Death Differ. 2025 Sep 22.
      Prostate cancer is one of the most prevalent malignancies in men, with increasing incidence and mortality largely attributed to treatment resistance and metastasis. The effectiveness of current therapies for advanced cases is hindered by intricate genetic and microenvironmental factors, emphasizing the urgent need for novel therapeutic targets. Chimeric RNAs have emerged as promising biomarkers in cancer research, among which CCDC719-13, a circular chimeric RNA, is frequently identified in prostate cancer. Our study reveals that CCDC719-13 expression is markedly reduced in advanced and recurrent prostate cancer, where its low levels serve as an independent predictor of poor prognosis. Functional experiments demonstrate that CCDC719-13 overexpression inhibits cell proliferation, induces apoptosis, and suppresses tumor growth in vivo, whereas its knockdown reverses these effects. Mechanistically, CCDC719-13 encodes a novel protein, CCDC7241aa, which triggers ferroptosis by interacting with SLC7A11 and facilitating its TRIM21-mediated ubiquitination and degradation. Notably, treatment with recombinant CCDC7241aa effectively suppresses tumor growth in patient-derived xenograft models without toxicity and enhances the efficacy of docetaxel and enzalutamide in vitro. These findings establish CCDC719-13 as a significant prognostic marker and potential therapeutic target in prostate cancer, with the recombinant CCDC7241aa protein offering promise for combination therapies in advanced cases.
    DOI:  https://doi.org/10.1038/s41418-025-01580-x
  15. Invest New Drugs. 2025 Sep 21.
      Mitochondrial dynamics, particularly the balance between fission and fusion, are critical in regulating cellular metabolism, apoptosis, and cancer progression. Dysregulation of this balance contributes to tumor survival and therapeutic resistance in castration-resistant prostate cancer (CRPC). Rucaparib, a clinically approved poly (ADP-ribose) polymerase (PARP) inhibitor, is primarily known for its role in DNA damage repair; however, its impact on mitochondrial function remains largely unexplored. In this study, we demonstrate that Rucaparib induces significant cytotoxicity and apoptosis in PC-3 CRPC cells in a time- and concentration-dependent manner, characterized by increased Bax/Bcl-2 ratio, cytochrome c release, and caspase-3 activation. Mechanistically, Rucaparib disrupts mitochondrial integrity by reducing mitochondrial membrane potential (MMP), inhibiting Complex IV activity, and depleting ATP levels. Confocal imaging and biochemical assays reveal that Rucaparib triggers mitochondrial fragmentation by promoting phosphorylation of dynamin-related protein 1 (Drp1) at Ser616 and enhancing its translocation to mitochondria. This process is accompanied by elevated intracellular Ca2+ levels and activation of calcium/calmodulin-dependent protein kinase II (CaMKII), suggesting a Ca2⁺/CaMKII/Drp1 signaling axis. Importantly, pharmacological inhibition of CaMKII with KN-93 reverses Drp1 mitochondrial translocation, restores mitochondrial morphology, and partially rescues ATP production, confirming the functional role of CaMKII in Rucaparib-induced mitochondrial dysfunction. These findings uncover a previously unrecognized mechanism of Rucaparib action beyond DNA repair inhibition, highlighting its ability to target mitochondrial dynamics and bioenergetics through Ca2+/CaMKII/Drp1 signaling. Our results provide new insights into the multifaceted anticancer mechanisms of Rucaparib and suggest that modulation of mitochondrial fission may offer a promising therapeutic avenue for CRPC.
    Keywords:  ATP; Castration-resistant prostate cancer (CRPC); Drp1; Mitochondrial dynamics; Rucaparib
    DOI:  https://doi.org/10.1007/s10637-025-01586-9
  16. Diseases. 2025 Sep 05. pii: 294. [Epub ahead of print]13(9):
      Prostate cancer (PCa) is the most common genitourinary malignancy in men, with a multifactorial etiology influenced by genetic, environmental, and microbial determinants. Although the prostate was traditionally considered sterile, advances in microbiome research have challenged this view, revealing potential links between microbial communities and PCa development, progression, and treatment response. This review synthesizes evidence on the gut, urinary, seminal fluid, and prostatic microbiomes, highlighting their potential contributions to PCa pathogenesis and therapeutic outcomes. Key studies utilizing next-generation sequencing (NGS), whole-genome sequencing (WGS), PCR, and metagenomic analyses have identified specific bacterial and fungal taxa associated with Pca; however, findings remain inconsistent across methodologies and cohorts. Microorganisms such as Propionibacterium acnes and Pseudomonas spp. may modulate inflammation, immune responses, and resistance to androgen-deprivation therapy. Further research is required to determine whether microbial signatures can serve as reliable biomarkers for early detection, prognosis, or novel therapeutic strategies in PCa management.
    Keywords:  gut microbiome; microbial biomarker; microbiota; next-generation sequencing; prostate cancer
    DOI:  https://doi.org/10.3390/diseases13090294
  17. Cell Death Differ. 2025 Sep 20.
      SPOP, the most frequently mutated gene in prostate cancer, has been implicated in the aberrant activation of stress granules, presenting significant challenges in disease management. However, the mechanistic link between SPOP mutations and cellular energy stress remains inadequately explored. In this study, we demonstrate that ULK1 expression is positively correlated with both loss-of-function mutations in SPOP and the upregulation of the E3 ubiquitin ligase TRIM24 in human prostate cancer specimens. Mechanistically, SPOP mutations induce the upregulation of TRIM24, which subsequently binds to ULK1 and catalyzes its non-degradative K27-linked polyubiquitylation. This post-translational modification enhances the stability of ULK1, facilitating cellular adaptation to energy stress and consequently promoting prostate cancer progression. Notably, pharmacological inhibition of TRIM24 using TRIM24-PROTAC (proteolysis-targeting chimera) effectively suppressed tumor growth in mice bearing SPOP-mutant prostate cancer cells. Collectively, these findings elucidate a pivotal role of SPOP mutations in modulating energy stress responses via TRIM24-mediated ULK1 ubiquitylation and underscore the therapeutic potential of targeting TRIM24 in SPOP-mutant prostate cancers.
    DOI:  https://doi.org/10.1038/s41418-025-01582-9
  18. Front Nutr. 2025 ;12 1646623
       Background: Global consumption of artificial sweeteners (ASs) has risen substantially in recent years. However, their relationship with prostate cancer (PCa) remains poorly characterized. This study investigates the AS-PCa association to identify pivotal genes potentially bridging this relationship.
    Method: This study retrieved target genes associated with ASs and PCa from multiple public databases. Protein-protein interaction (PPI) network analysis and visualization were conducted on overlapping genes, followed by the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses to explore the underlying mechanisms. Subsequently, the optimal predictive model was selected from 101 machine-learning algorithm combinations and validated against 2 external datasets. Molecular docking analysis was then performed to examine the interactions between key genes and AS compounds. Finally, in vitro cellular assays were conducted to validate the specific effects of ASs on PCa.
    Results: We analyzed seven common ASs-aspartame, acesulfame-K, sucralose, NHDC, sodium cyclamate, neotame, and saccharin-identifying 261 overlapping targets associated with PCa. The GO and KEGG enrichment analyses revealed that these targets primarily regulate cell proliferation, inflammation, and cancer cell metabolism. Machine learning algorithm screening identified the Lasso-SuperPC hybrid model as demonstrating optimal predictive performance, with robust validation in two independent external datasets. Subsequent analysis identified two key regulatory genes: CD38 and MMP11. Molecular docking analysis further confirmed potential interactions between AS compounds and the core target MMP11. Finally, in vitro cellular assays demonstrated that NHDC suppresses MMP11 expression in PCa cells and exhibits anti-PCa pharmacological effects.
    Conclusion: By integrating bioinformatics, machine learning, molecular docking, and in vitro cellular assays, this study demonstrates that ASs inhibit PCa progression through multiple molecular targets and signaling pathways. Collectively, these findings provide important insights into the safety assessment of food additives and cancer risk assessment.
    Keywords:  artificial sweetener; matrix metalloprotein 11; molecular docking; prostate cancer; robot learning
    DOI:  https://doi.org/10.3389/fnut.2025.1646623
  19. Urol Oncol. 2025 Sep 23. pii: S1078-1439(25)00314-X. [Epub ahead of print]
       BACKGROUND: The mutations in the Androgen Receptor (AR) known as H874Y in prostate cancer greatly influence cellular signaling and execute the cell proliferation. Phytochemicals of ginger (Zingiber officinale) extracted from methanol extract were investigated through multiple servers to identify the ADMET properties.
    METHODS: Our key considerations were on Gingerol and Gingerenone and their bindings with AR Prostate Cancer Mutant H874Y. Moreover, the molecular docking simulations, molecular dynamics, and simulations were executed to determine the key insight into the binding affinity, stability, and motions of the Prostate Cancer Mutant H874Y Ligand Binding Domain. In-vitro study was performed to evaluate the cytotoxicity of Zingiber officinale against 3 cell lines A549, MCF-7, and PC-3. Furthermore, cell nuclear morphology was analyzed using DAPI staining.
    RESULTS: The ADMET investigations revealed positive results concerning absorption, distribution, metabolism, and excretion with no signs of toxicity commenced and better binding affinity for Gingerol and Gingerenone-A. The molecular dynamics simulations were employed for the Prostate Cancer Mutant H874Y Ligand Binding Domain complexed Gingernone-A and Gingerol over 100 ns to identify the atomistic motions and stability of the desired ligands. The MD Simulations revealed that Gingernone-A was found stable, suggesting more consistent bindings and stability with higher hydrogen bond contacts during simulations. Moreover, the Gingerol was found equally stable to Gingernone-A confirmed by root mean square deviations (RMSD) which reflects the dynamic nature of the Gingerol. Furthermore, other parameters such as RMSF, and compactness were found within permissible limits. To validate the molecular docking simulations as well as molecular dynamics simulations the free energy was calculated from the whole trajectory obtained from the MD Simulations using the MM-PBSA method. Both Gingerol and Gingernone-A were found to be better modulators of the H874Y mutated ligand-binding domain with free binding energy for Gingerol -189.351 ± 1.272kJ/mol and Gingernone-A -322.881 ± 1.665 kJ/mol. Such negative binding energies provide an understanding of the binding nature of ligands with the template target. Moreover, the Gingerol with AR Prostate Cancer Ligand Binding Domain binding showed free binding energy -292.984 ± 2.673 kJ/mol. These negative binding energies illustrate the ligands' binding strengths. The results of in-vitro study showed good anticancer potential in methanol extract of Zingiber officinale against A549, MCF-7, and PC-3 cell lines with IC50 values of 464, 542, and 604 μg/mL respectively. The results of DAPI staining were showed remarkable changes in cell nuclear morphology.
    CONCLUSIONS: The results of current in-siico and in-vitro studies are important for gaining an understanding of the mechanisms of how the Zingiber officinale phytochemicals bind to the H874Y mutated ligand binding domain, which is important for the development of targeted therapy against Prostate Cancer Mutant H874Y.
    Keywords:  Free binding energy; Molecular docking; Molecular dynamics simulations; Prostate cancer mutant H874Y; Zingiber officinale
    DOI:  https://doi.org/10.1016/j.urolonc.2025.08.009
  20. Pharmaceuticals (Basel). 2025 Aug 27. pii: 1275. [Epub ahead of print]18(9):
      Background: Prostate cancer (PCa) is the primary contributor to male cancer-related mortality and currently lacks effective treatment options. The Modified Guizhi Fuling Decoction (MGFD) is used in clinical practice to treat multiple tumors. This research focused on the mechanisms of action (MOA) in MGFD that inhibit PCa. Methods: The impact of MGFD on PCa cells (PC3 and DU145) was examined via Cell Counting Kit-8, wound healing assays, and transwell assays. To determine the MOA, high-throughput sequencing based high-throughput screening (HTS2) was utilized along with network pharmacology. Results: The findings indicated that MGFD suppressed the proliferation, migration, and invasion of PCa cells. We then utilized the HTS2 assay to generate 270 gene expression profiles from PCa cells perturbed by MGFD. Large-scale transcriptional analysis highlighted three pathways closely associated with PCa: the TNF signaling pathway, cellular senescence, and FoxO signaling pathway. Through the combination of network pharmacology and bioinformatics, we discovered four primary targets through which MGFD acts on PCa: AKT serine/threonine kinase 1 (AKT1), Caspase-8 (CASP8), Cyclin-Dependent Kinase 1 (CDK1), and Cyclin D1 (CCND1). Finally, molecular docking demonstrated that the potential bioactive compounds baicalein, quercetin, and 5-[[5-(4-methoxyphenyl)-2-furyl] methylene] barbituric acid strongly bind to CDK1, AKT1, and CASP8, respectively. Conclusions: This research shows that MGFD displays encouraging anticancer effects via various mechanisms. Its multi-target activity profile underscores its promise as a potential therapeutic option for PCa treatment and encourages additional in vivo validation studies.
    Keywords:  HTS2 technology; Modified Guizhi Fuling Decoction; bioinformatics; network pharmacology; prostate cancer; transcriptomics
    DOI:  https://doi.org/10.3390/ph18091275
  21. J Environ Sci (China). 2026 Jan;pii: S1001-0742(25)00354-7. [Epub ahead of print]159 88-96
      Poly- and perfluoroalkyl substances (PFAS), including perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS), are persistent environmental pollutants with potential toxicological effects on human health. The aim of this study was to investigate the impact of PFOS and PFOA on the effectiveness of selected drugs used in the treatment of prostate cancer based on in vitro tests on cell lines. Three cell lines were used in the study: two human prostate cancer cells (DU-145 and PC3) and one human normal prostate cell line (PNT1A). Using dose-response experiments, it was observed that PFAS had differential effects on cancer and normal cells. At low concentrations, PFOA and PFOS stimulated the proliferation of cancer cells, particularly PC3, while higher concentrations led to reduced viability. In normal cells, PFOS exhibited greater cytotoxicity compared to PFOA. Furthermore, PFOS enhanced docetaxel cytotoxicity in PC3 cells but reduced its efficacy in DU-145 cells. Similarly, PFOA diminished cabazitaxel effectiveness in DU-145 cells, suggesting PFAS-drug interactions may depend on the cell type, drug, and PFAS concentration. Results suggest that PFAS may influence cellular processes through receptor-mediated pathways, oxidative stress modulation, and protein binding, altering drug bioavailability and cellular uptake. The study also highlights the non-monotonic dose-response relationships observed in PFAS-treated cells. These findings raise concerns about the potential risks associated with PFAS exposure, particularly in the context of cancer treatment. Future studies should focus on long-term, low-dose PFAS exposure, the use of primary cells, and the molecular mechanisms driving these interactions to better inform therapeutic strategies.
    Keywords:  Cell lines; In vitro; Poly- and perfluoroalkyl substances (PFAS); Prostate cancer; Toxicity
    DOI:  https://doi.org/10.1016/j.jes.2025.06.006
  22. Urol Oncol. 2025 Sep 20. pii: S1078-1439(25)00345-X. [Epub ahead of print]
    Uros Associats
       BACKGROUND: Microultrasound (microUS) is an emerging imaging modality that enables real-time, high-resolution prostate cancer detection.
    OBJECTIVES: To evaluate the diagnostic accuracy and clinical utility of microUS-targeted biopsies for the detection of clinically significant prostate cancer (csPCa) in a real-world cohort of patients with suspected disease.
    MATERIALS AND METHODS: We retrospectively analyzed 200 patients who underwent transperineal microUS-guided prostate biopsy between January 2022 and December 2024. All procedures were performed using the 29 MHz ExactVu system, applying the PRI-MUS scoring system for lesion characterization. Targeted biopsies were followed by 12-core systematic sampling. Diagnostic performance was assessed using sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV). Multivariate logistic regression was conducted to identify predictors of csPCa.
    RESULTS: Prostate cancer was detected in 124 patients (62.1%), with csPCa confirmed in 84 cases (42%). Lesions with PRI-MUS ≥4 were significantly associated with csPCa (P = 0.018), yielding a sensitivity of 93% and NPV of 83%. Among patients with negative or absent multiparametric magnetic resonance imaging (mpMRI) (n = 30), microUS identified csPCa in 16.7%. ISUP grade concordance between targeted biopsies and final prostatectomy specimens was 84.8%. PRI-MUS score emerged as the strongest independent predictor of csPCa (OR: 2.96; P = 0.001). The overall complication rate was 4%, exclusively minor events.
    CONCLUSIONS: MicroUS-targeted biopsies demonstrate robust diagnostic performance in identifying csPCa, particularly with PRI-MUS scores ≥4. Its real-time imaging capabilities, broad accessibility, and short learning curve suggest that microUS may serve as a reliable alternative or adjunct to mpMRI in contemporary prostate cancer diagnostic pathways.
    Keywords:  Diagnosis; High-frequency; Microultrasound; Multiparametric magnetic resonance imaging; Prostate biopsy; Prostate cancer
    DOI:  https://doi.org/10.1016/j.urolonc.2025.08.018
  23. Biology (Basel). 2025 Aug 27. pii: 1135. [Epub ahead of print]14(9):
      Prostate cancer (PCa) progression is shaped by the tumour microenvironment, where hypoxia promotes aggressiveness and contributes to therapy resistance. Extracellular vesicles (EVs), secreted under hypoxia, can deliver modified bioactive cargo that reprograms recipient cells. This study examined whether EVs from hypoxia-conditioned metastatic PCa cells enhance malignant traits in cancerous and non-tumorigenic prostate cell lines via Wnt signalling and epithelial-mesenchymal transition (EMT). EVs from PC3 cells cultured under hypoxia (1% O2) or normoxia (21% O2) as control were applied to LNCaP (low metastatic potential) and PNT2 (non-tumorigenic) cells. PC3 hypoxia-derived EVs increased HIF-1α, upregulated mesenchymal markers (Vimentin, N-cadherin) and Wnt-related genes (Wnt3A, Wnt5A, Fzd7), and suppressed the epithelial marker E-cadherin. Functional assessment showed that LNCaP cells treated with PC3 hypoxia EVs showed greater motility and invasiveness, and PNT2 cells displayed transcriptomic reprogramming. These findings show that hypoxia-driven EVs can propagate pro-metastatic signalling in less aggressive and normal prostate cells. The findings highlight EVs as a potential therapeutic target in PCa progression.
    Keywords:  HIF-1α; Wnt signalling (Wnt); epithelial–mesenchymal transition (EMT); extracellular vesicles (EVs); hypoxia; invasion; prostate cancer; tumour microenvironment
    DOI:  https://doi.org/10.3390/biology14091135
  24. Sci Rep. 2025 Sep 26. 15(1): 33076
      Despite extensive prior research on prostate cancer (PCa) transcriptomics, the molecular mechanisms underlying the disease's progression, particularly in the castration-resistant or metastatic stages, remain incompletely understood. The majority of recent research has concentrated on bulk RNA sequencing, which could mask the variation found in tumor microenvironments. This study aims to address this gap by integrating single-cell RNA sequencing (scRNA-seq) and bulk RNA sequencing with weighted gene co-expression network analysis (WGCNA) to investigate the molecular mechanisms of PCa at a higher resolution. In order to further individualized treatment plans for PCa, we aim to discover important genes and signaling pathways that could be used as therapeutic targets. We first preprocessed expression profile data from prostate cancer tissue samples, selecting 9,809 high-quality cells from a dataset. Following batch correction with Harmony and dimensionality reduction with principal component analysis (PCA), we used the Louvain clustering algorithm to divide the cells into discrete subtypes. The clusters were then visualized using t-SNE. This resulted in 16 cellular subtypes categorized into five major cell types: epithelial cells, monocytes, endothelial cells, CD8 + T-cells, and fibroblasts. Analysis of receptor-ligand pairs uncovered significant interactions between monocytes and both tumor cells and endothelial cells. Applying the high-dimensional WGCNA (hdWGCNA) method to construct a gene co-expression network, we detected seven gene modules, four of which were highly expressed in tumor cell subtypes and contained 380 key genes. Combining pathway analysis, we ultimately screened six key genes: CNPY2, CPE, DPP4, IDH1, NIPSNAP3A, and WNK4. We used Cox univariate regression and least absolute shrinkage and selection operator (lasso) regression techniques to build a prognostic prediction model that included these six important genes based on clinical data gathered from PCa patients. The prognostic prediction model constructed in this study demonstrated excellent predictive performance in both the training set and an external validation set, with the high-risk group showing significantly lower overall survival (OS) than the low-risk group. Furthermore, there was a substantial correlation found between risk scores and several immune-related gene sets, chemotherapeutic drug sensitivity, and tumor immune infiltration. High- and low-risk groups exhibited significant differences in immune cell content, immune factor levels, and immune dysfunction. Further analysis revealed significant correlations between the expression levels of model genes and multiple disease-related genes. Through Gene Set Variation Analysis (GSVA) and Gene Set Enrichment Analysis (GSEA), we uncovered perturbations in multiple signaling pathways in high- and low-risk groups, potentially impacting the prognosis of PCa patients. This study uncovers key genes and signaling pathways in the prostate cancer tumor microenvironment, particularly genes such as CNPY2, CPE, DPP4, IDH1, NIPSNAP3A and WNK4, which have potential as therapeutic targets. Our findings provide new insights into personalized treatment strategies for PCa and warrant further clinical validation in the future.
    Keywords:  Immune evasion; Prostate cancer; Single-cell RNA sequencing; Therapeutic targets; Tumor microenvironment; Weighted gene co-expression network analysis
    DOI:  https://doi.org/10.1038/s41598-025-15682-6
  25. Eur J Nucl Med Mol Imaging. 2025 Sep 23.
       PURPOSE: Activation of androgen receptor (AR) signaling is a hallmark of prostate cancer. Dynamic changes in AR expression exacerbate AR heterogeneity throughout prostate cancer therapy. This study aims to develop a series of 68Ga-labeled Enzalutamide-based positron emission tomography (PET) tracers for AR imaging.
    METHODS: [68Ga]Ga-DOTA-FZAR-1, [68Ga]Ga-DOTA-FZAR-2, and [68Ga]Ga-DOTAGA-FZAR-3 were synthesized and the stability was analyzed in vitro. The AR specificity of the three radiotracers was assessed in vitro using AR-negative and AR-positive prostate cancer cell lines and in vivo using tumor xenograft-bearing mice. Moreover, the first-in-human evaluation of [68Ga]Ga-DOTA-FZAR-2 was conducted in eight patients with prostate cancer.
    RESULTS: [68Ga]Ga-DOTA-FZAR-1, [68Ga]Ga-DOTA-FZAR-2, and [68Ga]Ga-DOTAGA-FZAR-3 were successfully synthesized with a radiochemical purity of more than 99%, and had good stability in vitro. Cellular uptake assays revealed that the radiotracers had the highest, intermediate, and lowest uptake in LNCaP, 22Rv1, and PC-3 cells, respectively, strongly correlating with AR expression levels (P < 0.001). Consistent with cellular uptake, the radiotracers also exhibited a hierarchical uptake pattern (highest to lowest) in tumors of mice bearing LNCaP, 22Rv1 and PC-3 xenografts, respectively. In addition, all three radiotracers were primarily eliminated through the urinary system, as confirmed by ex vivo biodistribution studies. More importantly, first-in-human investigation showed safety and diagnostic value of [68Ga]Ga-DOTA-FZAR-2 in AR-associated prostate cancer patients.
    CONCLUSION: We developed and validated a series of 68Ga-labeled Enzalutamide-based PET tracers for AR imaging. Initial preclinical and clinical evidence indicate that [68Ga]Ga-DOTA-FZAR-2 enables noninvasive, whole-body, and dynamic monitoring of AR expression in prostate cancer patients throughout therapy.
    Keywords:  Androgen receptor; First-in-human; Gallium-68; PET; Prostate cancer
    DOI:  https://doi.org/10.1007/s00259-025-07577-5