Functional integration of the Ah receptor with RelB and IL-8 confers the pro-survival advantage to mammary epithelial cells of inflammatory breast tumors - Archive ouverte HAL Accéder directement au contenu
Article Dans Une Revue Archives of Biochemistry and Biophysics Année : 2011

Functional integration of the Ah receptor with RelB and IL-8 confers the pro-survival advantage to mammary epithelial cells of inflammatory breast tumors

Résumé

The aryl hydrocarbon receptor (AhR) has been best known for its role in mediating the toxicity of dioxin. Here we show that AhR overexpression is found among estrogen receptor (ER)α-negative human breast tumors and that its overexpression is positively correlated to that of the NF-κB subunit RelB and Interleukin (IL)-8. Increased DNA binding activity of the AhR and RelB is coupled to IL-8 overexpression in primary breast cancer tissue, which was also supported by in situ hybridization. Activation of AhR in vitro by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced IL-8 expression in MDA-MB 436 and MCF-7 cells in an AhR and RelB dependent manner. Consistently, downregulation of RelB or AhR by small interfering RNAs (siRNA) decreased the level of IL-8 but increased expression of ERα in vitro in MCF-7 cells. Our results strongly suggest that RelB and AhR have a critical role in the regulation of IL-8 and reveal a supportive role of RelB and AhR in the anti-apoptotic response in human breast cancer cells. AhR and RelB may present a novel therapeutic target for inflammatory driven breast carcinogenesis and tumor progression. Overexpression of pro-survival factors AhR and RelB may explain the process of the development of environmentally-induced type of breast cancers.

Domaines

Cancer
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hal-03002191 , version 1 (20-11-2020)

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Christoph Franz Adam Vogel, Wen Li, Dalei Wu, Jamie Miller, Colleen Sweeney, et al.. Functional integration of the Ah receptor with RelB and IL-8 confers the pro-survival advantage to mammary epithelial cells of inflammatory breast tumors. Archives of Biochemistry and Biophysics, 2011, 512 (1), pp.78-86. ⟨10.1016/j.abb.2011.05.011⟩. ⟨hal-03002191⟩
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