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Studies have shown that Emodin promotes apoptosis, inhibits DNA synthesis, and promotes free radical generation in breast, lung, and prostate cancers. Further, this agent has the ability to inhibit metastasis and increase the efficacy of other anti-cancer agents with minimal toxicity to normal cell.

Anthraquinones are phytoestrogens that have been demonstrated to possess anticancer properties through the inhibition of cell proliferation, the induction of apoptosis, and the prevention of metastasis [1]. The effects of the anthraquinone derivatives emodin and aloe-emodin have been extensively investigated in several cancer types through studies on their signaling targets. Emodin has been reported to sensitize Her2/neu-overexpressing lung cancer cells to chemotherapeutic treatments and to suppress Her2/neu-overexpressing breast cancer growth by inhibiting tyrosine kinase activity [32–34]. Notably, emodin has been shown to downregulate androgen receptor (AR) and inhibit prostate cancer growth [5], suggesting that there is a connection between anthraquinone derivatives and steroid receptor in hormone-related cancers. Although the estrogenic ability of emodin is higher than that of aloe-emodin, as determined by ERα binding studies, the antiproliferation effect of aloe-emodin is more efficient than that of emodin in breast cancer cells [7]. Kang et al. also showed that the cytotoxicity of aloe-emodin is higher in ERα-positive cells than in ERα-negative cells [7]. These observations suggest that aloe-emodin might be a stronger inhibitor of ERα-positive cancer cell growth than emodin.

https://cancerci.biomedcentral.com/articles/10.1186/s12935-019-0820-3#Sec1                                                   https://www.hindawi.com/journals/ecam/2013/376123/                                                                                     https://onlinelibrary.wiley.com/doi/abs/10.1002/med.20094

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