Modulation of prostate cancer genetic risk by omega-3 and omega-6 fatty acids

Isabelle M Berquin ¹, Younong Min , Ruping Wu

⁰Department of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.

The Journal of Clinical Investigation +

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July 4, 2007

View abstract on PubMed

Summary

Omega-3 fatty acids can reduce prostate cancer growth in genetically predisposed mice, while omega-6 fatty acids worsen it. This effect is linked to Bad-dependent apoptosis, highlighting gene-diet interactions in cancer development.

Area Of Science

Oncology
Nutritional Science
Molecular Biology

Background

Genetic alterations are established causes of cancer.
The role of dietary fat in cancer risk, especially in genetically predisposed individuals, remains unclear.
Epidemiological studies suggest omega-3 polyunsaturated fatty acids may reduce cancer incidence.

Purpose Of The Study

To investigate the influence of dietary polyunsaturated fatty acids (PUFAs) on prostate cancer risk.
To determine the effects of omega-3 and omega-6 fatty acids in a genetically defined mouse model of prostate cancer.

Main Methods

Utilized prostate-specific Pten-knockout mice, an immune-competent orthotopic model.
Administered diets with defined polyunsaturated fatty acid levels.
Analyzed tumor growth, histopathological progression, survival rates, and molecular markers including Bad and apoptosis.

Main Results

Omega-3 fatty acids reduced prostate tumor growth, slowed progression, and increased survival.
Omega-6 fatty acids demonstrated opposite effects on tumor growth and progression.
Introducing omega-3 desaturase mimicked the tumor-reducing effects of an omega-3 diet.
Tumors from omega-3 fed mice showed reduced phosphorylated Bad and increased apoptosis.
Bad knockdown abolished omega-3-induced cell death, while exogenous Bad restored sensitivity.

Conclusions

Dietary omega-3 and omega-6 fatty acids significantly modulate prostate cancer development in a genetically predisposed model.
The mechanism involves Bad-dependent apoptosis, suggesting a key role for this pathway.
Highlights the critical importance of gene-diet interactions in prostate cancer development and progression.

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