Exercise Does Not Counteract the Effects of a “Westernized” Diet on Prostate Cancer Xenografts

Vandersluis, Avi; Venier, Natalie; Colquhoun, Alexandra; Sugar, Linda; Pollak, Michael; Kiss, Alex; Fleshner, Neil; Klotz, Laurence; Venkateswaran, Vasundara

doi:10.1002/pros.22673

Cited by 9 publications

(11 citation statements)

References 44 publications

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“…Exercise interventions in rodents are typically divided into forced and voluntary exercise. [18][19][20][21][22] The degree of protection against cancer has been proposed to be proportional to the intensity of exercise, 23 suggesting that there is a critical dose of exercise required to observe an effect on tumorigenesis. The rodents are nocturnal and will run during the dark period with average running distances reported to range from 1.6 to 12.7 km/night per mouse, 12 with 1 study reporting running distances up to 150 km/wk per mouse.…”

Section: Mode Of Exercisementioning

confidence: 99%

Effects of Exercise on Tumor Physiology and Metabolism

Pedersen

Christensen²,

Højman³

2015

The Cancer Journal

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Exercise is a potent regulator of a range of physiological processes in most tissues. Solid epidemiological data show that exercise training can reduce disease risk and mortality for several cancer diagnoses, suggesting that exercise training may directly regulate tumor physiology and metabolism. Here, we review the body of literature describing exercise intervention studies performed in rodent tumor models and elaborate on potential mechanistic effects of exercise on tumor physiology. Exercise has been shown to reduce tumor incidence, tumor multiplicity, and tumor growth across numerous different transplantable, chemically induced or genetic tumor models. We propose 4 emerging mechanistic effects of exercise, including (1) vascularization and blood perfusion, (2) immune function, (3) tumor metabolism, and (4) muscle-to-cancer cross-talk, and discuss these in details. In conclusion, exercise training has the potential to be a beneficial and integrated component of cancer management, but has yet to fully elucidate its potential. Understanding the mechanistic effects of exercise on tumor physiology is warranted. Insight into these mechanistic effects is emerging, but experimental intervention studies are still needed to verify the cause-effect relationship between these mechanisms and the control of tumor growth.

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Section: Mode Of Exercisementioning

confidence: 99%

Effects of Exercise on Tumor Physiology and Metabolism

Pedersen

Christensen²,

Højman³

2015

The Cancer Journal

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“…They were housed in clean cages with unrestricted access to water and food, under a 12-h photoperiod and standard temperature. Rats were randomly divided [35,36] into the following 5 groups with 10 rats each: positive control group, negative control group, and 3 groups receiving enoxaparin at 40, 60, or 80 mg/ml concentrations. Enoxaparin (Lovenox) , and prepared as a cream at concentrations of 40, 60 and 80 mg/ml.…”

Section: Methodsmentioning

confidence: 99%

“…There is a high prevalence of breast cancer globally [32,33] and in Iran [34]. Moreover, breast cancer has clinical, psychological, and economic complications [36]. In light of contradictory results reported in relation to breast cancer [21-23, 26, 27], the purpose of our study was to assess the effect of enoxaparin on dimethylbenzanthraceneinduced breast cancer in rats.…”

Section: Introductionmentioning

confidence: 99%

Effects of Enoxaparin Emulsion on Dimethylbenzanthracene-induced Breast Cancer in Female Rats

Bolandpayeh

Hassanpour-Ezzati

Mousavi

2018

RMM

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Introduction: Enoxaparin is an anticoagulant medication. Anticoagulation inhibits tumor cell-mediated release of angiogenic proteins and diminishes angiogenic response. Angiogenesis is an important event in various cancers such as breast cancer. Angiogenesis provide oxygen and nutrients to tumor cells and causes tumor progression. The aim of the present study was to evaluate the anti-angiogenesis effect of an enoxaparin cream on breast cancer induced by dimethylbenzanthracene in rats. Methods: In this experimental in vivo study, 50 Wistar female rats were divided into negative control (vehicle), positive control (cream base), and 3 groups with enoxaparin treatment (40, 60, and 80 mg/ml). After one month of treatment along with breast cancer induction by dimethylbenzanthracene, breast tissue samples were isolated and stained with hematoxylin-eosin, and tumor growth suppression rate was calculated. Tumor size (length and width) was measured using a clipper, and the tumor volume was calculated using the following formula: V = (L × W × W)/2, where V is tumor volume, W is tumor width, L is tumor length. The data were analyzed using one-way ANOVA and Tukey’s post hoc test. Results: Tumor suppression was significantly increased in enoxaparin treatment groups compared to the positive control group (40 mg/ml of enoxaparin treated versus positive control group; P = 0.017, 60 mg/ml of enoxaparin treated versus positive control; P = 0.015, 40 mg/ml of enoxaparin treated versus positive control; P = 0.009, 60 mg/ml of enoxaparin treated versus 40 mg/ml of enoxaparin treated; P = 0.019, and 80 mg/ml of enoxaparin treated versus 40 mg/ml of enoxaparin treated; P = 0.011 in a dose-dependent manner. Conclusion: Enoxaparin inhibits breast cancer in a dose-dependent manner. The application of enoxaparin cream in patients with breast cancer may considerably reduce tumor growth.

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“…The most experienced models to assess the impact of dietary fats on prostate cancer growth were subcutaneous xenograft models [11,12,15,16,35,52,58].…”

Section: Various Preclinical Modelsmentioning

confidence: 99%

Research Evidence on High-Fat Diet-Induced Prostate Cancer Development and Progression

Narita

Nara

Sato

et al. 2019

JCM

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Although recent evidence has suggested that a high-fat diet (HFD) plays an important role in prostate carcinogenesis, the underlying mechanisms have largely remained unknown. This review thus summarizes previous preclinical studies that have used prostate cancer cells and animal models to assess the impact of dietary fat on prostate cancer development and progression. Large variations in the previous studies were found during the selection of preclinical models and types of dietary intervention. Subcutaneous human prostate cancer cell xenografts, such as LNCaP, LAPC-4, and PC-3 and genetic engineered mouse models, such as TRAMP and Pten knockout, were frequently used. The dietary interventions had not been standardized, and distinct variations in the phenotype were observed in different studies using distinct HFD components. The use of different dietary components in the research models is reported to influence the effect of diet-induced metabolic disorders. The proposed underlying mechanisms for HFD-induced prostate cancer were divided into (1) growth factor signaling, (2) lipid metabolism, (3) inflammation, (4) hormonal modulation, and others. A number of preclinical studies proposed that dietary fat and/or obesity enhanced prostate cancer development and progression. However, the relationship still remains controversial, and care should be taken when interpreting the results in a human context. Future studies using more sophisticated preclinical models are imperative in order to explore deeper understanding regarding the impact of dietary fat on the development and progression of prostate cancer.

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Exercise Does Not Counteract the Effects of a “Westernized” Diet on Prostate Cancer Xenografts

Cited by 9 publications

References 44 publications

Effects of Exercise on Tumor Physiology and Metabolism

Effects of Exercise on Tumor Physiology and Metabolism

Effects of Enoxaparin Emulsion on Dimethylbenzanthracene-induced Breast Cancer in Female Rats

Research Evidence on High-Fat Diet-Induced Prostate Cancer Development and Progression

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