Journal
FOOD AND CHEMICAL TOXICOLOGY
Volume 176, Issue -, Pages -Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2023.113783
Keywords
Polycyclic aromatic hydrocarbons (PAHs); Histone deacetylase inhibitor (HDACi); 12-dimethylbenz[a]anthracene; Chemokines; CD4+T cells
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Exposure to PAHs in food is closely linked to breast cancer, possibly due to changes in immunotoxicity and immune regulation. HDACis have been found to reshape the tumor immune microenvironment and have an anti-tumor effect. However, the immune regulatory mechanism of HDACis in PAH-induced breast tumors is still unclear.
Polycyclic aromatic hydrocarbons (PAHs) exposure in food is closely associated with the occurrence and development of breast cancer, which may attribute to altered immunotoxicity and immune regulation. Currently, cancer immunotherapy aims to promote tumor-specific T cell responses, especially CD4+T helper cells (Th) for anti-tumor immunity. The histone deacetylase inhibitors (HDACis) are found to exert an anti-tumor effect by reshaping the tumor immune microenvironment, but the immune regulatory mechanism of HDACis in PAHsinduced breast tumor remains elusive. Here, using established breast cancer models induced by 7,12-dimethylbenz[a]anthracene (DMBA), a potent carcinogenic agent of PAH, the novel HDACi, 2-hexyl-4-pentylene acid (HPTA) exhibited anti-tumor effect by activating T lymphocytes immune function. HPTA recruited CXCR3+CD4+T cells into chemokines CXCL9/10-enriched tumor sites, and the increased secretion of CXCL9/10 was regulated by the NF-kappa B-mediated pathway. Furthermore, HPTA promoted Th1 differentiation and assisted cytotoxic CD8+T cells in the elimination of breast cancer cells. These findings support the proposition of HPTA as a potential therapeutic in the treatment of PAHs-induced carcinogenicity.
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