Benzophenone-3 promotion of mammary tumorigenesis is diet-dependent
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Anastasia Kariagina1, Elena Morozova1, Reyhane Hoshyar1, Mark D. Aupperlee1, Mitchell A. Borin1, Sandra Z. Haslam2 and Richard C. Schwartz1
1 Breast Cancer and the Environment Research Program, Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI, USA
2 Breast Cancer and the Environment Research Program, Department of Physiology, Michigan State University, East Lansing, MI, USA
|Richard C. Schwartz,||email:||[email protected]|
|Sandra Z. Haslam,||email:||[email protected]|
Keywords: oxybenzone; benzophenone-3; mammary tumorigenesis; dietary animal fat; breast cancer
Received: October 08, 2020 Accepted: November 20, 2020 Published: December 01, 2020
Benzophenone-3 is a putative endocrine disrupting chemical and common ingredient in sunscreens. The potential of endocrine disrupting chemicals to act as agonists or antagonists in critical hormonally regulated processes, such as mammary gland development and mammary tumorigenesis, demands evaluation of its potential in promoting breast cancer. This study identifies the effects of BP-3 on mammary tumorigenesis with high-fat diet during puberty versus adulthood in Trp53-null transplant BALB/c mice. Benzophenone-3 exposure yielded levels in urine similar to humans subjected to heavy topical sunscreen exposure. Benzophenone-3 was protective for epithelial tumorigenesis in mice fed lifelong low-fat diet, while promotional for epithelial tumorigenesis in mice fed adult high-fat diet. Benzophenone-3 increased tumor cell proliferation, decreased tumor cell apoptosis, and increased tumor vascularity dependent on specific dietary regimen and tumor histopathology. Even in instances of an ostensibly protective effect, other parameters suggest greater risk. Although benzophenone-3 seemed protective on low-fat diet, spindle cell tumors arising in these mice showed increased proliferation and decreased apoptosis. This points to a need for further studies of benzophenone-3 in both animal models and humans as a potential breast cancer risk factor, as well as a more general need to evaluate endocrine disrupting chemicals in varying dietary contexts.
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