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Chemical Compound Review

CCRIS 5597     3-methylanthracene-1,8,9-triol

Synonyms: AG-J-60445, Ambap491-59-8, AC1L1UVW, LS-20394, CTK4J1116, ...
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Disease relevance of AI3-62089


High impact information on AI3-62089

  • Stat1, Stat3, and Stat5 were activated in mouse epidermis after treatment with different classes of tumor promoters, including 12-O-tetradecanoylphorbol-13-acetate (TPA), okadaic acid, and chrysarobin [4].
  • At optimal promoting doses, chrysarobin treatment produced a maximum number of papillomas that was approximately 1/3 that produced by TPA (6.4 versus 17.0 papillomas per mouse, respectively) [5].
  • In addition, chrysarobin treatment following 10 wk of TPA promotion did not enhance the progression of preexisting papillomas to carcinomas [5].
  • Following treatment with both chrysarobin and TPA, higher levels of epidermal DNA synthesis correlated closely with higher molar ratios of spermidine/spermine, indicating a strong relationship between epidermal spermidine levels and epidermal cell proliferation induced by both promoters [6].
  • Antipsoriatic anthrones with modulated redox properties. 2. Novel derivatives of chrysarobin and isochrysarobin--antiproliferative activity and 5-lipoxygenase inhibition [7].

Anatomical context of AI3-62089

  • Chrysarobin induced a significant infiltration of PMNs into the dermis of DBA/2 mice whereas in C57BL/6 mice there was only a slight dermal infiltration of PMNs [8].
  • Although not significantly different, maximum elevations in epidermal thickness, total number of nucleated epidermal cells, and dark basal keratinocytes (DCs) induced by 220 nmol chrysarobin occurred at 96 h after treatment, while those induced by 3.4 nmol TPA occurred at 48 h [3].
  • A single application of TPA but not chrysarobin resulted in a rapid translocation of protein kinase C (PKC) to the membrane; however, treatment with both promoters ultimately led to a time-dependent loss of PKC activity in both membrane and cytosol fractions [9].

Associations of AI3-62089 with other chemical compounds


Gene context of AI3-62089

  • A single topical treatment of either 12-O-tetradecanoylphorbol-13-acetate (TPA) or chrysarobin or a single full-thickness wound induced the expression of HB-EGF and AR in mRNA samples isolated from whole mouse skin [14].
  • Subsequently, 125I-EGF binding increased to approximately 200% of control in epidermal membrane preparations from both TPA- and chrysarobin-treated mice [9].
  • A single topical application of TPA or chrysarobin induced elevated levels of transforming growth factor-alpha (TGF-alpha) mRNA at 6 h or 15-24 h, respectively [9].
  • The peaks of Cx26 and Cx43 expression and Cx31.1 inhibition appeared 12 h after TPA application and 24 h after OA and chrysarobin application [15].
  • Total RNA was isolated from SENCAR mouse epidermis at various times after single topical treatments with TPA (3.4 nmol), chrysarobin (220 nmol), okadaic acid (2.5 nmol), and thapsigargin (8.5 nmol) [16].

Analytical, diagnostic and therapeutic context of AI3-62089


  1. Characterization of skin tumor promotion and progression by chrysarobin in SENCAR mice. Kruszewski, F.H., Conti, C.J., DiGiovanni, J. Cancer Res. (1987) [Pubmed]
  2. Mechanism of mouse skin tumor promotion by chrysarobin. DiGiovanni, J., Decina, P.C., Prichett, W.P., Cantor, J., Aalfs, K.K., Coombs, M.M. Cancer Res. (1985) [Pubmed]
  3. Histologic alterations produced by chrysarobin (1,8-dihydroxy-3-methyl-9-anthrone) in SENCAR mouse skin: relationship to skin tumor promoting activity. Kruszewski, F.H., Naito, M., Naito, Y., DiGiovanni, J. J. Invest. Dermatol. (1989) [Pubmed]
  4. Epidermal growth factor receptor-mediated activation of Stat3 during multistage skin carcinogenesis. Chan, K.S., Carbajal, S., Kiguchi, K., Clifford, J., Sano, S., DiGiovanni, J. Cancer Res. (2004) [Pubmed]
  5. Tumor progression in Sencar mouse skin as a function of initiator dose and promoter dose, duration, and type. Ewing, M.W., Conti, C.J., Kruszewski, F.H., Slaga, T.J., DiGiovanni, J. Cancer Res. (1988) [Pubmed]
  6. Alterations in epidermal polyamine levels and DNA synthesis following topical treatment with chrysarobin in SENCAR mice. Kruszewski, F.H., DiGiovanni, J. Cancer Res. (1988) [Pubmed]
  7. Antipsoriatic anthrones with modulated redox properties. 2. Novel derivatives of chrysarobin and isochrysarobin--antiproliferative activity and 5-lipoxygenase inhibition. Müller, K., Leukel, P., Ziereis, K., Gawlik, I. J. Med. Chem. (1994) [Pubmed]
  8. Comparison of the histological changes in the skin of DBA/2 and C57BL/6 mice following exposure to various promoting agents. Naito, M., Naito, Y., DiGiovanni, J. Carcinogenesis (1987) [Pubmed]
  9. Evidence for autocrine/paracrine growth stimulation by transforming growth factor-alpha during the process of skin tumor promotion. Imamoto, A., Beltrán, L.M., DiGiovanni, J. Mol. Carcinog. (1991) [Pubmed]
  10. Modulation of chrysarobin skin tumor promotion. DiGiovanni, J., Kruszewski, F.H., Chenicek, K.J. Carcinogenesis (1988) [Pubmed]
  11. Inhibition of chrysarobin skin tumor promotion in SENCAR mice by antioxidants. Battalora, M.S., Kruszewski, F.H., DiGiovanni, J. Carcinogenesis (1993) [Pubmed]
  12. Structure-activity relationships for epidermal ornithine decarboxylase induction and skin tumor promotion by anthrones. DiGiovanni, J., Kruszewski, F.H., Coombs, M.M., Bhatt, T.S., Pezeshk, A. Carcinogenesis (1988) [Pubmed]
  13. Anthralin, a non-TPA type tumor promoter, synergistically enhances phorbol ester-caused prostaglandin E2 release from primary cultured mouse epidermal cells. Aizu, E., Yamamoto, S., Kato, R. Jpn. J. Pharmacol. (1992) [Pubmed]
  14. Altered expression of epidermal growth factor receptor ligands in tumor promoter-treated mouse epidermis and in primary mouse skin tumors induced by an initiation-promotion protocol. Kiguchi, K., Beltrán, L., Rupp, T., DiGiovanni, J. Mol. Carcinog. (1998) [Pubmed]
  15. Effect of diverse tumor promoters on the expression of gap-junctional proteins connexin (Cx)26, Cx31.1, and Cx43 in SENCAR mouse epidermis. Budunova, I.V., Carbajal, S., Slaga, T.J. Mol. Carcinog. (1996) [Pubmed]
  16. Elevation of transforming growth factor-alpha mRNA and protein expression by diverse tumor promoters in SENCAR mouse epidermis. Kiguchi, K., Beltrán, L.M., You, J., Rho, O., DiGiovanni, J. Mol. Carcinog. (1995) [Pubmed]
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