Anticancer potential of emodin

Abstract

Keywords: angiogenesis apoptosis cell cycle arrest emodin traditional Chinese medicine (TCM) a b s t r a c t Traditional Chinese Medicine (TCM) is widely used in clinical research due to its low toxicity, low number of side effects, and low cost. Many components of common fruits and vegetables play well-documented roles as chemopreventive or chemotherapeutic agents that suppress tumorigenesis. Anthraquinones are commonly extracted from the Polygonaceae family of plants, e.g., Rheum palmatum and Rheum officinale. Some of the major chemical components of anthraquinone and its derivatives, such as aloe-emodin, danthron, emodin, chrysophanol, physcion, and rhein, have demonstrated potential anticancer properties. This review evaluates the pharmacological effects of emodin, a major component of Aloe vera. In particular, emodin demonstrates anti-neoplastic, anti-inflammatory, anti-angiogenesis, and toxicological potential for use in pharmacology, both in vitro and in vivo. Emodin demonstrates cytotoxic effects (e.g., cell death) through the arrest of the cell cycle and the induction of apoptosis in cancer cells. The overall molecular mechanisms of emodin include cell cycle arrest, apoptosis, and the promotion of the expression of hypoxia-inducible factor 1a, glutathione S-transferase P, N-acetyltransferase,and glutathione phase I and II detoxification enzymes while inhibiting angiogenesis, invasion, migration, chemical-induced carcinogen-DNA adduct formation, HER2/neu, CKII kinase, and p34cdc2 kinase in human cancer cells. Hopefully, this summary will provide information regarding the actions of emodin in cancer cells and broaden the application potential of chemotherapy to additional cancer patients in the future.

Efficacy of traditional Chinese medicine in treating cancer

“…The study reported that the fragmentation of DNA could be observed by a fluorescence microscope at 72 h and apoptosis frequently increased when the cells were in a three-dimensional compared to a two-dimensional culture. The research regarding the emodin azide methyl anthraquinone derivative (22) demonstrates that cytotoxic effects (such as cell death) are through the arrest of the cell cycle and the induction of apoptosis in cancer cells. The overall molecular mechanisms of emodin include cell cycle arrest and apoptosis, promote the expression of hypoxia-inducible factor 1α, glutathione S-transferase P and N-acetyltransferase, and induce glutathione phase I and II detoxification enzymes to inhibit angiogenesis, invasion, migration and chemical-induced carcinogen-DNA adduct formation.…”

Resveratrol enhanced FOXO3 phosphorylation via synergetic activation of SIRT1 and PI3K/Akt signaling to improve the effects of exercise in elderly rat hearts

“…There is a report that mitochondrial damage will trigger mitophagy in cardiomyocytes through HSP90 and CDC37 activation, but oxidative stress inhibits HSP90 activation and causes cell death with FOXO3 accumulation in the nuclei. FOXO3 is a transcription factor with a function in Fas/FADD signaling pathway protein production and cell death (Joo et al 2011;Paraiso et al 2012;Hsu and Chung 2012).…”

CuIIcomplex of emodin with improved anticancer activity as demonstrated by its performance on HeLa and Hep G2 cells

“…This is particularly important because the formation of ROS by emodin, shown to be of immense importance in the different mechanisms concerning the action of the compound on different cancer cell lines, decreases upon complex formation. [24][25][26][27] The complex probably has several other attributes or is able to improve upon the existing qualities of emodin as an anticancer agent, such as it being a kinase inhibitor (of protein kinases CK2, p56lck, Her-2/neu, and Janus-activated kinase 2). 25,28 Emodin was reported to inhibit several signaling pathways as well; the complex could perhaps do even better.…”

“…[24][25][26][27] One such mechanism involves the generation of reactive oxygen species (ROS) as a formidable pathway for antitumor activity. [24][25][26][27] For this reason, we decided to induce ROS in HeLa cells that were previously treated with emodin or [Cu II (emod) 2 ] 2À or NAC (N-acetyl cysteine) using H 2 O 2 ; NAC being used in the experiment as a control. This was done as mentioned in Section 2.5.…”

“…[21][22][23][24][25][26] As part of our continuing effort to simplify anthracyclines and to improve their established anticancer activity, we decided to prepare a Cu(II) complex of emodin for the reasons mentioned above. 16,[18][19][20][24][25][26][27][28][29][30][31][32][33] Complexes of emodin have been prepared before but few researchers attempted to see if the metal-bound emodin was able to improve upon its existing attributes as an anticancer agent. 34 This study tries to show by comparison that the complex formation of emodin is benecial, as well as discusses aspects related to the structure, structure-activity relationships, biophysical interactions with DNA that were performed at different ionic strengths and temperatures, and a probable mechanism of action for emodin and its Cu(II) complex on cancer cells pertaining to the generation of reactive oxygen species (ROS).…”