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The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
Published on: November 30, 2016
Aerobic exercise training attenuates the deleterious effects of walker-256 cancer: effects on physical capacity,
Luis F Rodrigues1, Bruno R A Pelozin1, Edilamar M Oliveira1
1Laboratory of Biochemistry and Molecular Biology of Exercise, School of Physical Education and Sport, University of São Paulo, São Paulo, Brazil.
Background:
Aerobic exercise training (AET) is widely recognized for its preventive and therapeutic efficacy in chronic non-communicable diseases. Although studies have shown that AET delays tumor growth and cachexia in Walker-256 tumor-bearing rats, little is known about the impact of AET on cardiac phenotypes in different cancer models. Therefore, the aim of this study was to investigate cancer cachexia-induced cardiac changes in Walker-256 tumor and to analyze the therapeutic effects of AET on these changes.
Methods:
Wistar (n= 24) male rats were assigned into 3 groups: Wistar control (WC), control tumor (WCT), and tumor trained (WTT). Walker-256 tumor cells were subcutaneously injected into cancer groups to establish a robust cancer cachexia model. Swimming exercise training lasted 60 min, 5×/week/6 weeks, with 5% body weight workload. We assessed: exercise tolerance, hemodynamic parameters, tumor growth and cachexia, skeletal muscle and left ventricular mass by ratio of tissue weight/tibia length. Cardiac morphology and function were evaluated by echocardiography.
Results:
Walker-256 tumor induced exercise intolerance in the WCT group (267.65 ± 53.55 m; p < 0.05) compared to the WC group (455.77 ± 50.22 m). In contrast, AET prevented the exercise intolerance in the WTT group (578.63 ± 66.84 m) compared to control. WTT group showed a reduction in tumor weight (25.08 ± 4.05 g; p < 0.001) and the percentage of cachexia (7.83 ± 1.75%; p < 0.05) compared to the WCT group (47.08 ± 6 g/13.75 ± 1.71%), indicating a greater evolution of tumor growth and body weight loss in relation to trained group. Skeletal muscle wasting (soleus, gastrocnemius, plantaris and tibial anterior) was observed in cancer cachexia compared to control. In this way, Walker-256 tumor exhibited cardiac remodeling characterized by cardiac atrophy. AET reversed soleus and plantaris atrophy and led to significant anti-cardiac remodeling evaluated by LV mass in Walker-256 tumor.
Conclusion:
Our data provides a robust model of cancer cachexia, as well as highlights the effects of AET as a preventive strategy for mitigating the exercise intolerance, tumor growth, cachectic status, and the cardiac damage in Walker- 256 tumor.
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