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The anthraquinones emodin and aloe-emodin are abundant in rhubarb. Several lines of evidence indicate that emodin and aloe-emodin have estrogenic activity as phytoestrogens. However, their effects on estrogen receptor   α   (ER  α  ) activation and breast cancer cell growth remain controversial. The goal of this study is to investigate the effects and molecular mechanisms of emodin and aloe-emodin on breast cancer cell proliferation. Our results indicate that both emodin and aloe-emodin are capable of inhibiting breast cancer cell proliferation by downregulating ER  α   protein levels, thereby suppressing ER  α   transcriptional activation. Furthermore, aloe-emodin treatment led to the dissociation of heat shock protein 90 (HSP90) and ER  α   and increased ER  α   ubiquitination. Although emodin had similar effects to aloe-emodin, it was not capable of promoting HSP90/ER  α   dissociation and ER  α   ubiquitination. Protein fractionation results suggest that aloe-emodin tended to induce cytosolic ER  α   degradation. Although emodin might induce cytosolic ER  α   degradation, it primarily affected nuclear ER  α   distribution similar to the action of estrogen when protein degradation was blocked. In conclusion, our data demonstrate that emodin and aloe-emodin specifically suppress breast cancer cell proliferation by targeting ER  α   protein stability through distinct mechanisms. These findings suggest a possible application of anthraquinones in preventing or treating breast cancer in the future.

Emodin and Aloe-Emodin Suppress Breast Cancer Cell Proliferation through ERαInhibition