Obesity and prostate cancer: A narrative review

Wilson, Rebekah L.; Taaffe, Dennis R.; Newton, Robert U.; Hart, Nicholas; Lyons‐Wall, Philippa; Galvão, Daniel A.

doi:10.1016/j.critrevonc.2021.103543

Cited by 56 publications

(33 citation statements)

References 107 publications

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“…Obesity is a major risk factor for PC development and progression [ 9 ], as well as a driver of intestinal dysbiosis, which can be defined as an imbalance in the microbes present in the microflora. Dysbiosis is often associated with an increase in gut permeability and endotoxinemia, which is an increase in the circulating level of bacterial lipopolysaccharide (LPS) [ 10 , 11 ].…”

Section: Contribution Of the Intestinal Microbiota To Prostate Carcin...mentioning

confidence: 99%

Effects of the intestinal microbiota on prostate cancer treatment by androgen deprivation therapy

Terrisse¹,

Zitvogel²,

Kroemer³

2022

Microb Cell

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Prostate cancer (PC) can be kept in check by androgen deprivation therapy (ADT, usually with the androgen synthesis inhibitor abiraterone acetate or the androgen receptor antagonist such as enzalutamide) until the tumor evolves to castration-resistant prostate cancer (CRPC). The transition of hormone-sensitive PC (HSPC) to CPRC has been explained by cancer cell-intrinsic resistance mechanisms. Recent data indicate that this transition is also marked by cancer cell-extrinsic mechanisms such as the failure of ADT-induced PC immunosurveillance, which depends on the presence of immunostimulatory bacteria in the gut. Moreover, intestinal bacteria that degrade drugs used for ADT, as well as bacteria that produce androgens, can interfere with the efficacy of ADT. Thus, specific bacteria in the gut serve as a source of testosterone, which accelerates prostate cancer progression, and men with CRPC exhibit an increased abundance of such bacteria with androgenic functions. In conclusion, the response of PC to ADT is profoundly influenced by the composition of the microbiota with its immunostimulatory, immunosuppressive and directly ADT-subversive elements.

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Section: Contribution Of the Intestinal Microbiota To Prostate Carcin...mentioning

confidence: 99%

Effects of the intestinal microbiota on prostate cancer treatment by androgen deprivation therapy

Terrisse¹,

Zitvogel²,

Kroemer³

2022

Microb Cell

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“… 2 Obesity is a chronic condition that leads to numerous other serious diseases. 3 , 4 , 5 , 6 , 7 The etiology and progression of obesity involve a complex multifactorial interaction of genetic, biological, and environmental components. 4 , 8 Long‐term energy imbalance where energy intake (EI) exceeds energy expenditure (EE) results in obesity.…”

Section: Introductionmentioning

confidence: 99%

The combined effect of metformin and mirabegron on diet‐induced obesity

Zhao

Liu

Zhang

et al. 2023

MedComm

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Anti‐obesity medications act by suppressing energy intake (EI), promoting energy expenditure (EE), or both. Metformin (Met) and mirabegron (Mir) cause weight loss by targeting EI and EE, respectively. However, anti‐obesity effects during concurrent use of both have yet to be explored. In this study, we investigated the anti‐obesity effects, metabolic benefits, and underlying mechanisms of Met/Mir combination therapy in two clinically relevant contexts: the prevention model and the treatment model. In the prevention model, Met/Mir caused further 12% and 14% reductions in body weight (BW) gain induced by a high‐fat diet compared to Met or Mir alone, respectively. In the treatment model, Met/Mir additively promoted 17% BW loss in diet‐induced obese mice, which was 13% and 6% greater than Met and Mir alone, respectively. Additionally, Met/Mir improved glucose tolerance and insulin sensitivity. These benefits of Met/Mir were associated with increased EE, activated brown adipose tissue thermogenesis, and white adipose tissue browning. Significantly, Met/Mir did not cause cardiovascular dysfunction in either model. Together, the combination of Met and Mir could be a promising approach for the prevention and treatment of obesity by targeting both EI and EE simultaneously.

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“…The obese adipose environment is characterized by chronic inflammation driven in part by increased macrophage infiltration and elevated cytokine and adipokine expression [ 21 ]. This results in perturbed immune response and metabolic irregularities [ 22 , 23 ]. This chronic inflammatory state leads to chemoresistance, dysregulated angiogenesis, promotion of cancer cell growth, and the development of metastasis [ 22 , 23 , 24 ].…”

Section: Introductionmentioning

confidence: 99%

“…This results in perturbed immune response and metabolic irregularities [ 22 , 23 ]. This chronic inflammatory state leads to chemoresistance, dysregulated angiogenesis, promotion of cancer cell growth, and the development of metastasis [ 22 , 23 , 24 ]. Obesity has been shown to alter the gene expression profiles of periprostatic adipose tissue, creating an environment that favors prostate cancer progression by promoting cancer cell proliferation and immune escape [ 25 , 26 ].…”

Section: Introductionmentioning

confidence: 99%

Adipose Tissue-Derived Extracellular Vesicles Contribute to Phenotypic Plasticity of Prostate Cancer Cells

Mathiesen¹,

Haynes²,

Huyck³

et al. 2023

IJMS

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Metastatic prostate cancer is one of the leading causes of male cancer deaths in the western world. Obesity significantly increases the risk of metastatic disease and is associated with a higher mortality rate. Systemic chronic inflammation can result from a variety of conditions, including obesity, where adipose tissue inflammation is a major contributor. Adipose tissue endothelial cells (EC) exposed to inflammation become dysfunctional and produce a secretome, including extracellular vesicles (EV), that can impact function of cells in distant tissues, including malignant cells. The aim of this study was to explore the potential role of EVs produced by obese adipose tissue and the ECs exposed to pro-inflammatory cytokines on prostate cancer phenotypic plasticity in vitro. We demonstrate that PC3ML metastatic prostate cancer cells exposed to EVs from adipose tissue ECs and to EVs from human adipose tissue total explants display reduced invasion and increased proliferation. The latter functional changes could be attributed to the EV miRNA cargo. We also show that the functional shift is TWIST1-dependent and is consistent with mesenchymal-to-epithelial transition, which is key to establishment of secondary tumor growth. Understanding the complex effects of EVs on prostate cancer cells of different phenotypes is key before their intended use as therapeutics.

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Obesity and prostate cancer: A narrative review

Cited by 56 publications

References 107 publications

Effects of the intestinal microbiota on prostate cancer treatment by androgen deprivation therapy

Effects of the intestinal microbiota on prostate cancer treatment by androgen deprivation therapy

The combined effect of metformin and mirabegron on diet‐induced obesity

Adipose Tissue-Derived Extracellular Vesicles Contribute to Phenotypic Plasticity of Prostate Cancer Cells

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