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Inherent aerobic capacity-dependent differences in breast carcinogenesis
Henry J Thompson1, Lee W Jones2, Lauren G Koch3
1Cancer Prevention Laboratory, Colorado State University, Fort Collins, CO 80523-1173, USA.
Carcinogenesis
|September 16, 2017
Summary
High inherent aerobic capacity (HIAC) significantly reduced breast cancer incidence and multiplicity in rodent models. This protective effect appears linked to metabolic signaling pathways, suggesting a genetic influence on cancer risk.
Area of Science:
- Genetics and Cancer Biology
- Metabolic Signaling Pathways
- Rodent Models of Carcinogenesis
Background:
- Physical activity improves aerobic capacity and lowers breast cancer risk.
- Heritable traits influence aerobic capacity improvements from exercise.
- The impact of genetic factors on cancer risk, specifically breast cancer, remains under-evaluated.
Purpose of the Study:
- To investigate the role of heritable fitness in breast carcinogenesis.
- To evaluate the effect of inherent aerobic capacity on cancer development in the absence of physical activity.
- To explore the underlying metabolic mechanisms of protection.
Main Methods:
- Utilized N:NIH rats selectively bred for low (LIAC) or high (HIAC) inherent aerobic capacity.
- Administered 1-methyl-1-nitrosurea to induce breast cancer.
- Analyzed cancer incidence, multiplicity, body fat, and key protein signaling pathways (Akt, AMPK).
Main Results:
- HIAC rats exhibited significantly lower cancer incidence (14.0% vs 47.3%) and multiplicity (0.18 vs 0.85 cancers/rat) compared to LIAC rats.
- HIAC rats had reduced visceral and subcutaneous fat depots.
- HIAC was associated with suppressed Akt and activated AMPK signaling.
Conclusions:
- Heritable high aerobic capacity confers significant protection against chemically induced breast cancer in rats.
- The protective effect is partly mediated by alterations in core metabolic signaling pathways, including those involving Akt and AMPK.
- These findings suggest a genetic component to breast cancer risk that can be influenced by inherent metabolic profiles.
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