Increasing knowledge of the immunosuppressive tumor microenvironment in cancer-related processes has led to the developing of novel immune-based therapies that have changed the cancer treatment paradigm. In the tumor microenvironment, the plethora of soluble factors secreted by tumor cells interacts with immune cells and non-immune components to deliver signals necessary for tumor progression. Accordingly, targeting tumor-derived factors inducing this immunosuppressive tumor microenvironment has become an appealing therapeutic potential in advancing cancer treatment. CCL20, a chemokine best known to induce leucocyte migration in response to pathological and inflammatory conditions, has been implicated in tumor proliferation, angiogenesis, metastasis, immunosuppression, and therapeutic resistance. Notably, CCL20 and its receptor CCR6 are important in tumor microenvironment interactions. This review discusses the interaction between the CCL20–CCR6 axis and the tumor microenvironment and how these interactions promote tumor progression. Also, an outline of studies utilizing CCL20 in combination with other standard cancer treatments has been shed.

Although patients with early localized prostate cancer can survive longer, castration-resistant prostate cancer (CRPC) has gradually emerged with the use of androgen deprivation therapy (ADT). N-Myc and TEM8 play a vital role in the progression of several cancer types. However, the underlying mechanism of how N-Myc and TEM8 promote the progression of prostate cancer remains unclear. In this study, the expression of N-Myc and TEM8 was detected in benign prostatic hyperplasia (BPH) and prostate cancer (PCa) tissues by immunohistochemistry (IHC). LNCaP cell lines were maintained in RPMI 1640 medium supplemented with 10% charcoal-stripped fetal bovine serum. Subsequently, R language software was used to verify our results. Tubule formation assay of human umbilical vein endothelial cell (HUVEC) was conducted to examine the effect of N-Myc and TEM8 overexpression on angiogenesis in prostate cancer cells. IHC results showed a positive correlation between the expression of N-Myc and TEM8 in prostate cancer tissues. Further analysis showed that N-Myc and TEM8 were associated with clinicopathological features and poor prognosis in prostate cancer patients. Moreover, the overexpression of N-Myc and TEM8 promoted proliferation of prostate cancer cells and angiogenesis. Additionally, N-Myc and TEM8 overexpression was associated with therapeutic resistance. We further found that N-Myc promoted angiogenesis and therapeutic resistance in prostate cancer via TEM8. Hence, targeting N-Myc/TEM8 pathway in prostate cancer would be a novel therapeutic strategy to enhance the treatment of prostate cancer patients.

Prostate cancer (PCa) remains one of the leading causes of cancer-related morbidity and mortality in men worldwide, and therapeutic resistance—particularly to immunotherapy—continues to limit clinical efficacy. Mounting evidence has positioned the immunosuppressive tumor microenvironment (TME) as a core driver of disease progression and a formidable barrier to effective immune-based interventions. In this review, we present a comprehensive and multi-dimensional analysis of the cellular, stromal, and molecular constituents of the immunosuppressive TME in PCa, highlighting its significant heterogeneity and context-dependent functions. We emphasize recent breakthrough insights obtained through single-cell RNA sequencing (scRNA-seq), spatial multi-omics, and high-dimensional imaging technologies, which are redefining our understanding of tumor–immune–stromal interactions. Based on these mechanistic findings, we examine precision therapeutic strategies aimed at remodeling the TME, including combinatorial immune checkpoint blockade, metabolic reprogramming, cytokine network regulation, and advanced nanomedicine-based delivery systems. Finally, we discuss translational opportunities and future research directions, underscoring the necessity of integrating advanced omics technologies with biomarker-driven clinical trial design to enable individualized, precision interventions and improve survival outcomes for patients with PCa.