Mechanistic Insights and Therapeutic Advances in the Prostate Tumor Microenvironment

Dear Colleagues,

Prostate cancer (PCa) remains a leading cause of cancer-related death among men and is characterized by complex interactions between tumor cells and their surrounding microenvironment. Composed of fibroblasts, immune cells, endothelial cells, pericytes, and neural elements, the tumor microenvironment (TME) is critical in disease progression, therapeutic resistance, and metastasis. Cancer-associated fibroblasts (CAFs) promote tumor growth, invasion, and immune suppression through the dynamic remodeling of the extracellular matrix and secretion of growth factors. Tumor-associated macrophages (TAMs) and other immune cells contribute to an immunosuppressive milieu, enabling immune evasion and resistance to therapy. In addition, metabolic stressors such as hypoxia and acidosis shape cellular behavior in the TME, inducing treatment resistance and tumor aggressiveness. Interactions with neural components, including sympathetic and parasympathetic nerves, have additionally been implicated in tumor progression and metastatic spread.

We seek original research and reviews that study in vitro, ex vivo, or in vivo TME models, utilizing novel methods and asking thought-provoking questions in examining the role of the TME and its potential as a therapeutic target in prostate cancer.

This Special Issue aims to highlight recent advances in understanding the cellular and molecular mechanisms by which the prostate TME supports cancer development, progression, and therapy resistance.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following:

• Cellular and molecular components of the prostate tumor microenvironment;
• Mechanisms of immune evasion and immunosuppression in the prostate TME;
• The role of cancer-associated fibroblasts (CAFs) in tumor progression and therapy resistance;
• Metabolic reprogramming and adaptation within the TME;
• Crosstalk between tumor cells and the stromal or neural microenvironment;
• Hypoxia, acidosis, and other microenvironmental stressors shaping tumor behavior;
• Lineage plasticity promoted by the TME;
• The influence of the TME on metastatic tropism and organ-specific colonization;
• TME contributions to racial and molecular disparities in prostate cancer;
• Targeting the TME with immunotherapies, stromal modulators, or metabolic interventions;
• The use of novel 3D organoids, ex vivo cultures, and in vivo models to study the prostate TME.

We look forward to receiving your contributions.

Dr. Omar E. Franco
Guest Editor

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