Emodin inhibits breast tumorigenesis in the comorbidity of hyperlipidemia and associated with IL-17 suppression.
[BACKGROUND] This study explored the interaction between breast cancer and the hyperlipidemia microenvironment, and assessed the anti-tumorigenic effects of the natural compound Emodin.
APA
Liu Q, Zheng L, et al. (2026). Emodin inhibits breast tumorigenesis in the comorbidity of hyperlipidemia and associated with IL-17 suppression.. Biochemistry and biophysics reports, 45, 102520. https://doi.org/10.1016/j.bbrep.2026.102520
MLA
Liu Q, et al.. "Emodin inhibits breast tumorigenesis in the comorbidity of hyperlipidemia and associated with IL-17 suppression.." Biochemistry and biophysics reports, vol. 45, 2026, pp. 102520.
PMID
41799696
Abstract
[BACKGROUND] This study explored the interaction between breast cancer and the hyperlipidemia microenvironment, and assessed the anti-tumorigenic effects of the natural compound Emodin.
[METHODS] The human cancer atlas and gene expression databases were used to identify links between breast cancer and hyperlipidemia. Oxidized LDL (oxLDL) stimulation and high-fat diet (HFD) feeding were used to simulate hyperlipidemia. Quantitative PCR, flow cytometry, IF/IHC staining, FPLC and biological experiments were conducted to evaluate Emodin's efficacy. Molecular docking simulation and molecular dynamic analysis were used to identify potential targets of Emodin.
[RESULTS] Lipid metabolism mediators CD36 and IL-17 activation were associated with breast cancer development. Bioinformatics identified IL-17 priming cytokines, and experiments confirmed Emodin inhibited Th17-priming cytokines after oxLDL stimulation. Emodin modulated tumorigenic genes especially apoptosis, inhibited breast cancer cell stemness and migration, and reduced tumor growth in HFD-feeding wild-type (WT) mice. Emodin reduced macrophage infiltration, angiogenesis, and IL-17 expression in tumors. Molecular docking and dynamic analysis suggested potential targets (IL17RA and TNFR1) for Emodin in modulating breast cancer development in hyperlipidemia microenvironment.
[CONCLUSION] Emodin effectively reduced tumorigenesis in HFD mice, accompanied with inhibited IL-17 expression and suppressed macrophage infiltration. This result provided evidence for the pro-tumorigenic role of hyperlipidemia in breast cancer development, and support the natural compound Emodin as a promising anti-tumor agent with targeting IL-17 signaling molecules.
[METHODS] The human cancer atlas and gene expression databases were used to identify links between breast cancer and hyperlipidemia. Oxidized LDL (oxLDL) stimulation and high-fat diet (HFD) feeding were used to simulate hyperlipidemia. Quantitative PCR, flow cytometry, IF/IHC staining, FPLC and biological experiments were conducted to evaluate Emodin's efficacy. Molecular docking simulation and molecular dynamic analysis were used to identify potential targets of Emodin.
[RESULTS] Lipid metabolism mediators CD36 and IL-17 activation were associated with breast cancer development. Bioinformatics identified IL-17 priming cytokines, and experiments confirmed Emodin inhibited Th17-priming cytokines after oxLDL stimulation. Emodin modulated tumorigenic genes especially apoptosis, inhibited breast cancer cell stemness and migration, and reduced tumor growth in HFD-feeding wild-type (WT) mice. Emodin reduced macrophage infiltration, angiogenesis, and IL-17 expression in tumors. Molecular docking and dynamic analysis suggested potential targets (IL17RA and TNFR1) for Emodin in modulating breast cancer development in hyperlipidemia microenvironment.
[CONCLUSION] Emodin effectively reduced tumorigenesis in HFD mice, accompanied with inhibited IL-17 expression and suppressed macrophage infiltration. This result provided evidence for the pro-tumorigenic role of hyperlipidemia in breast cancer development, and support the natural compound Emodin as a promising anti-tumor agent with targeting IL-17 signaling molecules.
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