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Chemical Compound Review

emodin     1,3,8-trihydroxy-6-methyl- anthracene-9,10...

Synonyms: Emodol, Schuttgelb, LS-3, Lopac-E-7881, S2295_Selleck, ...
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Disease relevance of Rheum emodin

  • Suppressed transformation and induced differentiation of HER-2/neu-overexpressing breast cancer cells by emodin [1].
  • Our work indicates a new mechanism for the emodin-mediated anticancer effect and justifies further investigation of emodin as a therapeutic and preventive agent for prostate cancer [2].
  • The selected clones were expressed in Escherichia coli (BM 25.8 line) and were further screened for biosynthesis of emodin to hypericin, which resulted in an 84.6% conversion [3].
  • Furthermore, the combination of emodin with cisplatin, doxorubicin or etoposide (VP16) synergistically inhibited the proliferation of HER-2/neu-overexpressing lung cancer cells, whereas low doses of emodin, cisplatin, doxorubicin, or VP16 alone had only minimal antiproliferative effects on these cells [4].
  • In vivo study showed that emodin made the EC/CUHK1 cell-derived tumors more sensitive to arsenic trioxide with no additional systemic toxicity and side effects [5].

High impact information on Rheum emodin


Chemical compound and disease context of Rheum emodin


Biological context of Rheum emodin

  • Here, we first found that emodin significantly inhibited cell adhesion of various human cancer cells [6].
  • Emodin enters the nucleotide binding site of the enzyme, filling a hydrophobic pocket between the N-terminal and the C-terminal lobes, in the proximity of the site occupied by the base rings of the natural co-substrates [13].
  • The replacement of ATP by the competitive inhibitor emodin induces conformational modifications in the catalytic site of protein kinase CK2 [13].
  • In this study a novel red-color-based colony screening method for examining a cDNA library (lambda-TriplEX2) derived from H. perforatum cell cultures revealed the gene responsible for hypericin biosynthesis after the administration of emodin, a precursor of hypericin [3].
  • In contrast, emodin, which blocks phosphorylation of her2/neu by heregulin, failed to reduce NF-kappaB activation [14].

Anatomical context of Rheum emodin


Associations of Rheum emodin with other chemical compounds

  • A combination of CK2 inhibitors, emodin or 4,5,6,7-tetrabromobenzotriazole, with octreotide was injected intraperitoneally from postnatal (P) day P11 to P17 to block mouse OIR [18].
  • The work described here was carried out to examine (1) whether the tyrosine kinase activity of p185neu is required for resistance to chemotherapeutic drugs of HER-2/neu-overexpressing NSCLC cells and (2) whether the tyrosine kinase inhibitor emodin can sensitize these cells to chemotherapeutic drugs [4].
  • A group of chrysophanol and emodin derivatives with DNA-intercalating capability and with or without alkylating potential have been synthesized and shown to have antitumor activity in vitro [19].
  • Proteasome-dependent degradation of endogenous Id1 in HeLa cells is also stimulated by treatment with curcumin or emodin [20].
  • Such induction was ameliorated by emodin (20 microg/mL) (TGF-beta 1 concentration 2.25 +/- 0.15 and 2.96 +/- 0.33 pg/microg cellular protein at 24 hours and 48 hours, respectively, in the presence of emodin and 30 mmol D-glucose; P < 0.001 compared to 30 mmol D-glucose alone at both time points) [21].

Gene context of Rheum emodin


Analytical, diagnostic and therapeutic context of Rheum emodin


  1. Suppressed transformation and induced differentiation of HER-2/neu-overexpressing breast cancer cells by emodin. Zhang, L., Chang, C.J., Bacus, S.S., Hung, M.C. Cancer Res. (1995) [Pubmed]
  2. Emodin down-regulates androgen receptor and inhibits prostate cancer cell growth. Cha, T.L., Qiu, L., Chen, C.T., Wen, Y., Hung, M.C. Cancer Res. (2005) [Pubmed]
  3. Molecular and biochemical characterization of an enzyme responsible for the formation of hypericin in St. John's wort (Hypericum perforatum L.). Bais, H.P., Vepachedu, R., Lawrence, C.B., Stermitz, F.R., Vivanco, J.M. J. Biol. Chem. (2003) [Pubmed]
  4. Sensitization of HER-2/neu-overexpressing non-small cell lung cancer cells to chemotherapeutic drugs by tyrosine kinase inhibitor emodin. Zhang, L., Hung, M.C. Oncogene (1996) [Pubmed]
  5. Anthraquinones sensitize tumor cells to arsenic cytotoxicity in vitro and in vivo via reactive oxygen species-mediated dual regulation of apoptosis. Yang, J., Li, H., Chen, Y.Y., Wang, X.J., Shi, G.Y., Hu, Q.S., Kang, X.L., Lu, Y., Tang, X.M., Guo, Q.S., Yi, J. Free Radic. Biol. Med. (2004) [Pubmed]
  6. Emodin inhibits tumor cell adhesion through disruption of the membrane lipid Raft-associated integrin signaling pathway. Huang, Q., Shen, H.M., Shui, G., Wenk, M.R., Ong, C.N. Cancer Res. (2006) [Pubmed]
  7. Emodin enhances arsenic trioxide-induced apoptosis via generation of reactive oxygen species and inhibition of survival signaling. Yi, J., Yang, J., He, R., Gao, F., Sang, H., Tang, X., Ye, R.D. Cancer Res. (2004) [Pubmed]
  8. Tyrosine kinase inhibitor emodin suppresses growth of HER-2/neu-overexpressing breast cancer cells in athymic mice and sensitizes these cells to the inhibitory effect of paclitaxel. Zhang, L., Lau, Y.K., Xia, W., Hortobagyi, G.N., Hung, M.C. Clin. Cancer Res. (1999) [Pubmed]
  9. Intercalating agents with covalent bond forming capability. A novel type of potential anticancer agents. 2. Derivatives of chrysophanol and emodin. Koyama, M., Takahashi, K., Chou, T.C., Darzynkiewicz, Z., Kapuscinski, J., Kelly, T.R., Watanabe, K.A. J. Med. Chem. (1989) [Pubmed]
  10. Inhibition of electron transfer and uncoupling effects by emodin and emodinanthrone in Escherichia coli. Ubbink-Kok, T., Anderson, J.A., Konings, W.N. Antimicrob. Agents Chemother. (1986) [Pubmed]
  11. Investigations on DNA binding in rat liver and in Salmonella and on mutagenicity in the Ames test by emodin, a natural anthraquinone. Bösch, R., Friederich, U., Lutz, W.K., Brocker, E., Bachmann, M., Schlatter, C. Mutat. Res. (1987) [Pubmed]
  12. Inhibition of phosphorylation of p38 MAPK involved in the protection of nephropathy by emodin in diabetic rats. Wang, J., Huang, H., Liu, P., Tang, F., Qin, J., Huang, W., Chen, F., Guo, F., Liu, W., Yang, B. Eur. J. Pharmacol. (2006) [Pubmed]
  13. The replacement of ATP by the competitive inhibitor emodin induces conformational modifications in the catalytic site of protein kinase CK2. Battistutta, R., Sarno, S., De Moliner, E., Papinutto, E., Zanotti, G., Pinna, L.A. J. Biol. Chem. (2000) [Pubmed]
  14. Identification of signal transduction pathways involved in constitutive NF-kappaB activation in breast cancer cells. Bhat-Nakshatri, P., Sweeney, C.J., Nakshatri, H. Oncogene (2002) [Pubmed]
  15. Emodin (3-methyl-1,6,8-trihydroxyanthraquinone) inhibits TNF-induced NF-kappaB activation, IkappaB degradation, and expression of cell surface adhesion proteins in human vascular endothelial cells. Kumar, A., Dhawan, S., Aggarwal, B.B. Oncogene (1998) [Pubmed]
  16. Tyrosine kinase inhibitors, emodin and its derivative repress HER-2/neu-induced cellular transformation and metastasis-associated properties. Zhang, L., Lau, Y.K., Xi, L., Hong, R.L., Kim, D.S., Chen, C.F., Hortobagyi, G.N., Chang, C., Hung, M.C. Oncogene (1998) [Pubmed]
  17. Emodin inhibits tumor cell migration through suppression of the phosphatidylinositol 3-kinase-Cdc42/Rac1 pathway. Huang, Q., Shen, H.M., Ong, C.N. Cell. Mol. Life Sci. (2005) [Pubmed]
  18. Expression of protein kinase CK2 in astroglial cells of normal and neovascularized retina. Kramerov, A.A., Saghizadeh, M., Pan, H., Kabosova, A., Montenarh, M., Ahmed, K., Penn, J.S., Chan, C.K., Hinton, D.R., Grant, M.B., Ljubimov, A.V. Am. J. Pathol. (2006) [Pubmed]
  19. Topoisomerase II-mediated DNA cleavage activity and irreversibility of cleavable complex formation induced by DNA intercalator with alkylating capability. Kong, X.B., Rubin, L., Chen, L.I., Ciszewska, G., Watanabe, K.A., Tong, W.P., Sirotnak, F.M., Chou, T.C. Mol. Pharmacol. (1992) [Pubmed]
  20. Ubiquitin-dependent degradation of Id1 and Id3 is mediated by the COP9 signalosome. Berse, M., Bounpheng, M., Huang, X., Christy, B., Pollmann, C., Dubiel, W. J. Mol. Biol. (2004) [Pubmed]
  21. Emodin ameliorates glucose-induced matrix synthesis in human peritoneal mesothelial cells. Chan, T.M., Leung, J.K., Tsang, R.C., Liu, Z.H., Li, L.S., Yung, S. Kidney Int. (2003) [Pubmed]
  22. Emodin inhibits vascular endothelial growth factor-A-induced angiogenesis by blocking receptor-2 (KDR/Flk-1) phosphorylation. Kwak, H.J., Park, M.J., Park, C.M., Moon, S.I., Yoo, D.H., Lee, H.C., Lee, S.H., Kim, M.S., Lee, H.W., Shin, W.S., Park, I.C., Rhee, C.H., Hong, S.I. Int. J. Cancer (2006) [Pubmed]
  23. A novel function of emodin: enhancement of the nucleotide excision repair of UV- and cisplatin-induced DNA damage in human cells. Chang, L.C., Sheu, H.M., Huang, Y.S., Tsai, T.R., Kuo, K.W. Biochem. Pharmacol. (1999) [Pubmed]
  24. Involvement of protein kinase CK2 in angiogenesis and retinal neovascularization. Ljubimov, A.V., Caballero, S., Aoki, A.M., Pinna, L.A., Grant, M.B., Castellon, R. Invest. Ophthalmol. Vis. Sci. (2004) [Pubmed]
  25. Synthesis and active oxygen generation by new emodin derivatives and their gonadotropin-releasing hormone conjugates. Lev-Goldman, V., Mester, B., Ben-Aroya, N., Koch, Y., Weiner, L., Fridkin, M. Bioconjug. Chem. (2006) [Pubmed]
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