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Exploring Molecular Mechanisms of Prostate Cancer
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Exploring Molecular Mechanisms of Prostate Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 June 2026 | Viewed by 2109

Special Issue Editor

Dr. Estefania Labanca

E-Mail Website
Guest Editor
Department of Genitourinary Medical Oncology and The David H. Koch Center for Applied Research of Genitourinary Cancers, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
Interests: prostate cancer; bone metastasis; tumor microenvironment; tumor-host interaction; therapy resistance; progression mechanisms; patient-derived xenografts; cancer modeling

Special Issue Information

Dear Colleagues,

Prostate cancer is a clinically heterogeneous disease with distinct subtypes and molecular pathways involved. Progression to lethality includes genomic and epigenomic alterations affecting androgen receptor (AR), DNA repair, cell cycle, and signaling pathways. Low mutation rates highlight critical drivers of aberrant cell function like AR variants, microRNAs, and tumor-microenvironment interactions.

This Special Issue aims to illuminate the key mechanisms underlying prostate cancer development, progression, and resistance. Contributions exploring emerging diagnostics, AR signaling, non-coding RNAs, epigenetic regulation, and tumor ecosystem interplay are encouraged. By integrating genetics, transcriptomics, metabolomics, and therapeutic research insights, it seeks to foster novel strategies to advance precision oncology.

Dr. Estefania Labanca
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • genetic alterations
  • signlaing pathways
  • cellular dysregulation
  • non-coding RNAs
  • epigenetics
  • tumor microenvironment
  • metabolic factors
  • therapuetic targeting
  • multi-modal approaches

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Published Papers (2 papers)

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24 pages, 3973 KB  
Article
Ectopic FGFR1 Increases Intracellular Pool of Cholesterol in Prostate Cancer Cells
by Ziying Liu, Yuepeng Ke, Tingting Hong, Kennedy Smith, Peter Davies, Yun Huang, Dekai Zhang, Sanjukta Chakraborty, Yubin Zhou and Fen Wang
Int. J. Mol. Sci. 2026, 27(3), 1190; https://doi.org/10.3390/ijms27031190 - 24 Jan 2026
Cited by 1 | Viewed by 1090
Abstract
Prostate cancer (PCa) is the most common male cancer and the second leading cause of cancer death in men. Androgen deprivation therapy (ADT) has been widely used as the first-line treatment for PCa. However, most PCa will progress to castration-resistant PCa (CRPC) that [...] Read more.
Prostate cancer (PCa) is the most common male cancer and the second leading cause of cancer death in men. Androgen deprivation therapy (ADT) has been widely used as the first-line treatment for PCa. However, most PCa will progress to castration-resistant PCa (CRPC) that resists ADT 1 to 3 years after the treatment. Steroidogenesis from cholesterol is one of the mechanisms leading to ADT resistance. In PCa cells, low-density lipoprotein (LDL) mediated uptake is the major venue to acquire cholesterol. However, the mechanism of regulating this process is not fully understood. Fibroblast growth factor receptor 1 (FGFR1) is a receptor tyrosine kinase (RTK) that is ectopically expressed in PCa cells and promotes PCa progression by activating downstream signaling pathways. To comprehensively determine the roles of FGFR1 in PCa, we generated FGFR1-null DU145 cells and compared the transcriptomes of FGFR1-null and wild-type cells. We found that ablation of FGFR1 reduced the expression of genes promoting LDL uptake and de novo synthesis of cholesterol, thereby reducing the overall cholesterol pool in PCa cells. Detailed mechanistic studies further revealed that FGFR1 boosted the activation of sterol regulatory element-binding protein 2 (SREBP2) through ERK-dependent phosphorylation and cleavage, which, in turn, increased the expression of low-density lipoprotein receptor (LDLR) and enzymes involved in de novo cholesterol synthesis. Furthermore, in silico analyses demonstrated that high expression of FGFR1 was associated with high LDLR expression and clinicopathological features in PCa. Collectively, our data unveiled a previously unrecognized therapeutic avenue for CRPC by targeting FGFR1-driven cholesterol uptake and de novo synthesis. Full article
(This article belongs to the Special Issue Exploring Molecular Mechanisms of Prostate Cancer)
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21 pages, 5916 KB  
Article
An Interferon-Response Transcriptomic Signature of Lymphovascular Invasion in Prostate Cancer
by Cagdas Aktan, Christina M. Breneman, Okan Argun, Nora Seeley, Ceren Atalar, Kendall Robinson, Ari S. Hilibrand, Sophia Li, Swati Mamidanna and Mutlay Sayan
Int. J. Mol. Sci. 2026, 27(5), 2167; https://doi.org/10.3390/ijms27052167 - 25 Feb 2026
Viewed by 602
Abstract
Lymphovascular invasion is an adverse pathologic feature in prostate cancer, but its independent molecular drivers remain unclear due to strong confounding by tumor grade and stage. We performed a confounder-adjusted transcriptomic analysis of 403 TCGA-PRAD samples. Differential expression was adjusted for Gleason score [...] Read more.
Lymphovascular invasion is an adverse pathologic feature in prostate cancer, but its independent molecular drivers remain unclear due to strong confounding by tumor grade and stage. We performed a confounder-adjusted transcriptomic analysis of 403 TCGA-PRAD samples. Differential expression was adjusted for Gleason score and pathological T stage. A transcriptional profile associated with LVI was derived and tested in multivariable logistic and Cox proportional hazards models for biochemical recurrence-free survival, with bootstrap internal validation. After multivariable adjustment, 129 genes were independently associated with LVI. This gene set was overwhelmingly enriched for interferon-alpha/beta signaling and antiviral response pathways. A continuous composite score derived from this profile predicted a reduced risk of biochemical recurrence independently of standard clinicopathological factors (adjusted HR per unit = 0.911, 95% CI: 0.835–0.993, p = 0.033). Multi-omics integration revealed subtle promoter hypomethylation and strong correlations between methylation and expression for key interferon genes, supporting transcriptional regulation. We identify a robust, interferon-response transcriptional profile that specifically defines LVI in prostate cancer after accounting for major clinical confounders. This transcriptional signature provides independent prognostic information, refines the biological understanding of LVI, and presents a novel targetable pathway for further investigation. Full article
(This article belongs to the Special Issue Exploring Molecular Mechanisms of Prostate Cancer)
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