scholarly journals Periprostatic Adipose Tissue and Prostate Cancer Progression: New Insights into the Tumor Microenvironment

2014 ◽  
Vol 12 (1) ◽  
pp. 21-26 ◽  
Author(s):  
Paul Toren ◽  
Vasundara Venkateswaran
Keyword(s):  
Prostate Cancer ◽  
Adipose Tissue ◽  
Tumor Microenvironment ◽  
Cancer Progression ◽  
Prostate Cancer Progression

scholarly journals Regulation of prostate cancer progression by the tumor microenvironment

2016 ◽  
Vol 380 (1) ◽  
pp. 340-348 ◽  
Author(s):  
Stephen L. Shiao ◽  
Gina Chia-Yi Chu ◽  
Leland W.K. Chung
Keyword(s):  
Prostate Cancer ◽  
Tumor Microenvironment ◽  
Cancer Progression ◽  
Prostate Cancer Progression

scholarly journals Linking obesogenic dysregulation to prostate cancer progression

2015 ◽  
Vol 4 (4) ◽  
pp. R68-R80 ◽  
Author(s):  
Renea A Taylor ◽  
Jennifer Lo ◽  
Natasha Ascui ◽  
Matthew J Watt
Keyword(s):  
Prostate Cancer ◽  
Adipose Tissue ◽  
Cancer Progression ◽  
Prostate Gland ◽  
The Body ◽  
Endocrine Function ◽  
Low Grade ◽  
Prostate Cancer Progression ◽  
Cancer Aggressiveness ◽  
Increased Risk

The global epidemic of obesity is closely linked to the development of serious co-morbidities, including many forms of cancer. Epidemiological evidence consistently shows that obesity is associated with a similar or mildly increased incidence of prostate cancer but, more prominently, an increased risk for aggressive prostate cancer and prostate cancer-specific mortality. Studies in mice demonstrate that obesity induced by high-fat feeding increases prostate cancer progression; however, the mechanisms underpinning this relationship remain incompletely understood. Adipose tissue expansion in obesity leads to local tissue dysfunction and is associated with low-grade inflammation, alterations in endocrine function and changes in lipolysis that result in increased delivery of fatty acids to tissues of the body. The human prostate gland is covered anteriorly by the prominent peri-prostatic adipose tissue and laterally by smaller adipose tissue depots that lie directly adjacent to the prostatic surface. We discuss how the close association between dysfunctional adipose tissue and prostate epithelial cells might result in bi-directional communication to cause increased prostate cancer aggressiveness and progression. However, the literature indicates that several ‘mainstream’ hypotheses regarding obesity-related drivers of prostate cancer progression are not yet supported by a solid evidence base and, in particular, are not supported by experiments using human tissue. Understanding the links between obesity and prostate cancer will have major implications for the health policy for men with prostate cancer and the development of new therapeutic or preventative strategies.

scholarly journals Arginine and Arginases Modulate Metabolism, Tumor Microenvironment and Prostate Cancer Progression

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4503
Author(s):  
Andreia Matos ◽  
Marcos Carvalho ◽  
Manuel Bicho ◽  
Ricardo Ribeiro
Keyword(s):  
Prostate Cancer ◽  
Tumor Microenvironment ◽  
Cancer Progression ◽  
Urea Cycle ◽  
Suppressor Cells ◽  
Myeloid Derived Suppressor Cells ◽  
Prostate Cancer Progression ◽  
Arginine Metabolism ◽  
Arginine Deprivation ◽  
The Impact

Arginine availability and activation of arginine-related pathways at cancer sites have profound effects on the tumor microenvironment, far beyond their well-known role in the hepatic urea cycle. Arginine metabolism impacts not only malignant cells but also the surrounding immune cells behavior, modulating growth, survival, and immunosurveillance mechanisms, either through an arginase-mediated effect on polyamines and proline synthesis, or by the arginine/nitric oxide pathway in tumor cells, antitumor T-cells, myeloid-derived suppressor cells, and macrophages. This review presents evidence concerning the impact of arginine metabolism and arginase activity in the prostate cancer microenvironment, highlighting the recent advances in immunotherapy, which might be relevant for prostate cancer. Even though further research is required, arginine deprivation may represent a novel antimetabolite strategy for the treatment of arginine-dependent prostate cancer.

Exosomes from the tumor microenvironment as reciprocal regulators that enhance prostate cancer progression

2016 ◽  
Vol 23 (9) ◽  
pp. 734-744 ◽  
Author(s):  
Che-Ming Liu ◽  
Chia-Ling Hsieh ◽  
Chia-Ning Shen ◽  
Cheng-Chieh Lin ◽  
Katsumi Shigemura ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Microenvironment ◽  
Cancer Progression ◽  
Prostate Cancer Progression

scholarly journals Sex steroids in the tumor microenvironment and prostate cancer progression

2018 ◽  
Vol 25 (3) ◽  
pp. R179-R196 ◽  
Author(s):  
Clovis Boibessot ◽  
Paul Toren
Keyword(s):  
Prostate Cancer ◽  
Tumor Microenvironment ◽  
Cancer Progression ◽  
Sex Steroids ◽  
Biological Effects ◽  
Basic Research ◽  
Prostate Tumor ◽  
Sex Steroid ◽  
Prostate Cancer Progression ◽  
The Relationship

Prostate cancer is uniquely dependent on androgens. Despite years of research on the relationship between androgens and prostate cancer, many questions remain as to the biological effects of androgens and other sex steroids during prostate cancer progression. This article reviews the clinical and basic research on the influence of sex steroids such as androgens, estrogens and progesterone within the prostate tumor microenvironment on the progression of prostate cancer. We review clinical studies to date evaluating serum sex steroids as prognostic biomarkers and discuss their respective biological effects within the prostate tumor microenvironment. We also review the link between genomic alterations and sex steroid levels within prostate tumors. Finally, we highlight the links between sex steroid levels and the function of the immune system within the tumor microenvironment. As the context of treatment of lethal prostate cancer evolves over time, an understanding of this underlying biology remains central to developing optimal treatment approaches.

scholarly journals Prostaglandin E2 Inhibits Prostate Cancer Progression by Countervailing Tumor Microenvironment-Induced Impairment of Dendritic Cell Migration through LXRα/CCR7 Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Kuang Youlin ◽  
He Weiyang ◽  
Liang Simin ◽  
Gou Xin
Keyword(s):  
Prostate Cancer ◽  
Immune Response ◽  
Dendritic Cells ◽  
Cell Migration ◽  
Dendritic Cell ◽  
Tumor Microenvironment ◽  
Cancer Progression ◽  
Prostaglandin E ◽  
Prostate Cancer Progression ◽  
Dendritic Cell Migration

Migration and homing of dendritic cells (DCs) to lymphoid organs are quite crucial for T cell-induced immune response against tumor. However, tumor microenvironment can make some tumor cells escape immune response by impairing DC migration. Prostaglandin E2 (PGE2) plays important roles in initiating and terminating inflammatory responses. In this study, we investigated whether PGE2 could inhibit murine prostate cancer progression by countervailing tumor microenvironment-induced impairment of dendritic cell migration. We found that murine prostate cancer cell line RM-1-conditioned medium impaired chemotactic movement of marrow-derived DCs and splenic cDCs toward CC chemokine receptor-7 (CCR7) ligand CCL19 in vitro and migration to draining lymph gland in vivo. Meanwhile, it also induced LXRα activation and CCR7 inhibition on maturing DCs. However, the treatment of PGE2 rescued this impairment of DC migration with upregulation of CCR7 and inhibition of LXRα. Further, it was observed that PGE2 also increased MMP9 expression and activated Notch1 signaling on DCs. In RM-1-bearing mouse model, PGE2 treatment was identified to inhibit tumor growth and induce more tumor-infiltrating T cells and CD11c dendritic cells in tumor sites. Therefore, our findings may demonstrate a new perspective for therapeutic interventions on prostate cancer immunoescape.

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