High Salt Intake Attenuates Breast Cancer Metastasis to Lung.

Abstract

Diet-related factors are thought to modify the risk of cancers, while the influence of high salt intake remains largely uncharacterized. Breast cancer is the most common cancer in women worldwide. In the present study, we examined the effect of salt intake on breast cancer by using a 4T1 mouse mammary tumor model. Unexpectedly, both the fitness and the survival rate of the tumor-bearing mice were improved by high salt intake. Similarly, high salt intake suppressed the primary tumor growth as well as metastasis to lung in mice. Mechanistically, high salt intake greatly reduced food intake and thus might exert antitumor effect through mimicking calorie restriction. Immunoblotting showed the lower proliferation marker Ki-67 and the higher expression of the tumor suppressor gene p53 in tumors of high salt intake mice. Importantly, high salt intake might induce hyperosmotic stress, which sensitized breast cancer cells to p53-dependent anoikis. Collectively, our findings raise the possibility that endogenous salt deposition might act as the first-line defense system against breast cancer progression as well as metastasis.

• Authors: Yijuan Xu, Wenzhe Wang, Minmin Wang, Xuejiao Liu, Mee-Hyun Lee, Mingfu Wang, Hao Zhang, Haitao Li, Wei Chen
• Journal: Journal of agricultural and food chemistry (J Agric Food Chem) Vol. 66 Issue 13 Pg. 3386-3392 (Apr 04 2018) ISSN: 1520-5118 [Electronic] United States
• PMID: 29553743 (Publication Type: Journal Article)

Chemical References

• Tumor Suppressor Protein p53
• Sodium Chloride

Topics

• Animals
• Breast Neoplasms (diet therapy, genetics, metabolism, pathology)
• Cell Line, Tumor
• Female
• Gene Expression Regulation, Neoplastic
• Humans
• Lung (metabolism, pathology)
• Lung Neoplasms (metabolism, pathology, secondary)
• Mice
• Mice, Inbred BALB C
• Neoplasm Metastasis (genetics, prevention & control)
• Sodium Chloride (metabolism)
• Tumor Suppressor Protein p53 (genetics, metabolism)