Abstract 3706: Intervention of human breast cell carcinogenesis chronically induced by 3, 4, 4’-trichlorocarbanilide.

Abstract

Abstract The purpose of this study was to investigate the ability of antimicrobial agent 3,4,4’-trichlorocarbanilide (TCC) to induce breast cell carcinogenesis, and then identify preventive agents to intervene in TCC-induced breast cell carcinogenesis. TCC is widely used in personal care products such as bath soaps, detergents, and cleansing lotions. Recent studies suggest that TCC acts as an endocrine disruptor to enhance the ability of steroid hormones (estrogen or testosterone) to induce estrogen and androgen receptor-mediated gene expression. Due to its environmental persistence and wide use, there are concerns about TCC's possible impact on human health. To determine whether TCC exposure may contribute to the development of breast cancer, we used our chronically-induced breast cell carcinogenesis model to determine the ability of TCC to induce progressive carcinogenesis of human breast epithelial MCF10A cells to acquire cancer-associated properties. We found that chronic exposure of MCF10A cells to TCC at physiologically-achievable nanomolar levels resulted in cellular acquisition of the cancer-associated properties of reduced dependence on growth factors, anchorage independent growth, and increased cell proliferation. These cellular changes were accompanied by upregulation of the ERK pathway, Nox1-induced ROS production, and DNA damage. We also found that curcumin, a component of turmeric extracted from the rhizome of the Indian herb Curcuma longa, was able to suppress TCC-induced cellular carcinogenesis. Our study revealed, for the first time, that chronic exposure to TCC was able to induce breast cell carcinogenesis, and TCC-induced cellular carcinogenesis was preventable by curcumin. Citation Format: Shilpa Sood, Shambhunath Choudhary, Hwa-Chain R. Wang. Intervention of human breast cell carcinogenesis chronically induced by 3, 4, 4’-trichlorocarbanilide. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3706. doi:10.1158/1538-7445.AM2013-3706