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Chemical Compound Review

NSC-51805     N-[2-[2-nitro-5- (trifluoromethyl)phenyl]su...

Synonyms: AC1L6ABG, AC1Q1XMU, NSC51805
 
 
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Disease relevance of cantharidin

  • Investigations of other phorbol esters revealed an excellent correlation between their promoting ability and their ability to induce epidermal hyperplasia; however, that was not the case for compounds outside the phorbol ester series (i.e., acetic acid, cantharidin, and ethylphenylpropiolate) [1].
  • First, the potency of 15 active cantharidin analogs for inhibiting [3H]cantharidin binding is correlated with their acute toxicity to mice (r = 0.829) [2].
  • NCTD is a demethylated form of cantharidin with antitumor properties, which is now in use as a routine anticancer drug against hepatoma [3].
  • Cantharidin is a natural toxin that has antitumor properties and causes leukocytosis as well as increasing sensitivity of tumor cells resistant to other chemotherapeutic agents [4].
  • These findings show the cardiotoxic properties of cantharidin and its ability to produce fatal cardiac arrhythmias [5].
 

High impact information on cantharidin

  • An NPA treatment that reduced basipetal transport in rcn1 and cantharidin-treated wild-type plants also restored a normal gravity response and asymmetric auxin-induced gene expression, indicating that increased basipetal auxin transport impedes gravitropism [6].
  • CBP dephosphorylation of phosphorylase alpha is sensitive not only to okadaic acid, as with PP2A, but also to cantharidin and its analogs, consistent with their potency in blocking the radioligand binding site of CBP [7].
  • The phosphatase 2A inhibitor, cantharidin (> or = 10 micromol/L), also blocked the IFN-gamma induction of the C1 INH gene [8].
  • Zinc, okadaic acid, calyculin A, cantharidin, and the caspase inhibitor z-VAD-fmk, all prevented the cleavage of D4-GDI, DNA digestion, and apoptosis [9].
  • Correlative studies conducted with established PPase inhibitors reveal that, when applied at concentrations that inhibit PPase activity to a comparable extent, both okadaic acid and cantharidin also induce aberrant centrosome replication, the appearance of multiple aberrant mitotic spindles, and G2-M-phase growth arrest [10].
 

Chemical compound and disease context of cantharidin

  • Papaverine salicylate (MR-800) has been tested as a topical antiinflammatory agent in several models of skin inflammation in rodents, such as mouse ear dermatitis induced by croton oil, cantharidin or zymosan, and rat paw oedema induced by PAF [11].
  • The aim of this study was to compare the in vitro effects of cantharidin and nor-cantharidin on renal toxicity and on inflammatory events associated with tumoural process where protein phosphatases could be involved (energy status, prostanoid production, glutathione and nitrite contents) on RAW 264.7 and LLC-PK1 cells [12].
  • Without heat pretreatment, similar attenuation of the HSP27 dephosphorylation/granulation and the actin cytoskeleton stability during simulated ischemia were achieved by treating cells with the protein phosphatase inhibitors cantharidin or sodium orthovanadate [13].
 

Biological context of cantharidin

  • By contrast, when okadaic acid or cantharidin, potent inhibitors of protein phosphatase 2A (PP2A), was applied to the cells, the S-phase-specific high level of telomerase activity was continuously maintained in the cell cycle for at least 14 h after release from M-phase arrest [14].
  • The phosphorylation was further elevated in combination with cantharidin, an inhibitor of type 1+2A protein phosphatases [15].
  • This shows that the peaks of S-phase cells seen at 16 and 28 h after cantharidin application represent mother and daughter cells, respectively, the latter still cycling in partial synchrony [16].
  • Our findings suggest that alterations in specific genes functionally related to cell proliferation or apoptosis may be responsible for cantharidin-mediated cytotoxicity [4].
  • Cells pulse-labeled in S phase 30 min prior to treatment with cantharidin or TPA were slightly delayed in their progression through S phase and temporarily blocked in G2 phase [17].
 

Anatomical context of cantharidin

 

Associations of cantharidin with other chemical compounds

 

Gene context of cantharidin

 

Analytical, diagnostic and therapeutic context of cantharidin

References

  1. Epidermal cell proliferation and promoting ability of phorbol esters. Slaga, T.J., Scribner, J.D., Viaje, A. J. Natl. Cancer Inst. (1976) [Pubmed]
  2. Partial characterization of specific cantharidin binding sites in mouse tissues. Graziano, M.J., Pessah, I.N., Matsuzawa, M., Casida, J.E. Mol. Pharmacol. (1988) [Pubmed]
  3. Effector mechanisms of norcantharidin-induced mitotic arrest and apoptosis in human hepatoma cells. Chen, Y.N., Chen, J.C., Yin, S.C., Wang, G.S., Tsauer, W., Hsu, S.F., Hsu, S.L. Int. J. Cancer (2002) [Pubmed]
  4. Analysis of gene expression profiles in human HL-60 cell exposed to cantharidin using cDNA microarray. Zhang, J.P., Ying, K., Xiao, Z.Y., Zhou, B., Huang, Q.S., Wu, H.M., Yin, M., Xie, Y., Mao, Y.M., Rui, Y.C. Int. J. Cancer (2004) [Pubmed]
  5. A model of cardiac arrhythmias and sudden death: cantharidin-induced toxic cardiomyopathy. Rabkin, S.W., Friesen, J.M., Ferris, J.A., Fung, H.Y. J. Pharmacol. Exp. Ther. (1979) [Pubmed]
  6. Genetic and chemical reductions in protein phosphatase activity alter auxin transport, gravity response, and lateral root growth. Rashotte, A.M., DeLong, A., Muday, G.K. Plant Cell (2001) [Pubmed]
  7. Cantharidin-binding protein: identification as protein phosphatase 2A. Li, Y.M., Casida, J.E. Proc. Natl. Acad. Sci. U.S.A. (1992) [Pubmed]
  8. Phosphatase 2A participates in interferon-gamma's induced upregulation of C1 inhibitor mRNA expression. Heda, G.D., Kehoe, K.J., Mahdi, F., Schmaier, A.H. Blood (1996) [Pubmed]
  9. Cleavage and nuclear translocation of the caspase 3 substrate Rho GDP-dissociation inhibitor, D4-GDI, during apoptosis. Krieser, R.J., Eastman, A. Cell Death Differ. (1999) [Pubmed]
  10. Fostriecin-mediated G2-M-phase growth arrest correlates with abnormal centrosome replication, the formation of aberrant mitotic spindles, and the inhibition of serine/threonine protein phosphatase activity. Cheng, A., Balczon, R., Zuo, Z., Koons, J.S., Walsh, A.H., Honkanen, R.E. Cancer Res. (1998) [Pubmed]
  11. Protective effects of papaverine salicylate in mouse ear dermatitis and PAF-induced rat paw oedema. de Bernardis, E., Leonardi, G., Caruso, A., Cutuli, V.M., Amico-Roxas, M. Agents Actions (1994) [Pubmed]
  12. In vitro assessment of renal toxicity and inflammatory events of two protein phosphatase inhibitors cantharidin and nor-cantharidin. Massicot, F., Dutertre-Catella, H., Pham-Huy, C., Liu, X.H., Duc, H.T., Warnet, J.M. Basic & clinical pharmacology & toxicology. (2005) [Pubmed]
  13. Early and delayed tolerance to simulated ischemia in heat-preconditioned endothelial cells: a role for HSP27. Loktionova, S.A., Ilyinskaya, O.P., Kabakov, A.E. Am. J. Physiol. (1998) [Pubmed]
  14. Cell cycle-dependent regulation of telomerase activity by auxin, abscisic acid and protein phosphorylation in tobacco BY-2 suspension culture cells. Yang, S.W., Jin, E., Chung, I.K., Kim, W.T. Plant J. (2002) [Pubmed]
  15. Activation and inactivation of cAMP-response element-mediated gene transcription in cardiac myocytes. Müller, F.U., Bokník, P., Knapp, J., Linck, B., Lüss, H., Neumann, J., Schmitz, W. Cardiovasc. Res. (2001) [Pubmed]
  16. Cell cycle progression kinetics of regenerating mouse epidermal cells: an in vivo study combining DNA flow cytometry, cell sorting, and [3H]dThd autoradiography. Clausen, O.P., Kirkhus, B., Schjølberg, A.R. J. Invest. Dermatol. (1986) [Pubmed]
  17. A comparison between the epidermal regenerative responses provoked by a skin irritant and a tumor promoter using anti-BrdUrd/DNA flow cytometry. Kirkhus, B., Olsen, W.M., Clausen, O.P. Carcinogenesis (1991) [Pubmed]
  18. Macrophage release of transforming growth factor beta1 during resolution of monosodium urate monohydrate crystal-induced inflammation. Yagnik, D.R., Evans, B.J., Florey, O., Mason, J.C., Landis, R.C., Haskard, D.O. Arthritis Rheum. (2004) [Pubmed]
  19. Activation of inducible nitric oxide synthase gene in murine macrophages requires protein phosphatases 1 and 2A activities. Dong, Z., Yang, X., Xie, K., Juang, S.H., Llansa, N., Fidler, I.J. J. Leukoc. Biol. (1995) [Pubmed]
  20. Investigation of the human macrophage. I. Collection and in vitro cultivation. Chang, Y.C., Yao, C.S. Eur. J. Immunol. (1979) [Pubmed]
  21. Transgenic plant cells lacking mitochondrial alternative oxidase have increased susceptibility to mitochondria-dependent and -independent pathways of programmed cell death. Robson, C.A., Vanlerberghe, G.C. Plant Physiol. (2002) [Pubmed]
  22. Interaction of angiotensin II with the angiotensin type 2 receptor inhibits the cardiac transient outward potassium current. Caballero, R., Gómez, R., Moreno, I., Nuñez, L., González, T., Arias, C., Guizy, M., Valenzuela, C., Tamargo, J., Delpón, E. Cardiovasc. Res. (2004) [Pubmed]
  23. Anti-inflammatory properties of an oxidized sterol. Gaspari, A.A., Rietschel, R.L. J. Invest. Dermatol. (1985) [Pubmed]
  24. Protein phosphatase in neuroblastoma cells: [3H]cantharidin binding site in relation to cytotoxicity. Laidley, C.W., Cohen, E., Casida, J.E. J. Pharmacol. Exp. Ther. (1997) [Pubmed]
  25. The effect of the protein phosphatases inhibitor cantharidin on beta-adrenoceptor-mediated vasorelaxation. Knapp, J., Bokník, P., Linck, B., Lüss, H., Müller, F.U., Nacke, P., Neumann, J., Vahlensieck, U., Schmitz, W. Br. J. Pharmacol. (1997) [Pubmed]
  26. Roles of p38 and JNK mitogen-activated protein kinase pathways during cantharidin-induced apoptosis in U937 cells. Huh, J.E., Kang, K.S., Chae, C., Kim, H.M., Ahn, K.S., Kim, S.H. Biochem. Pharmacol. (2004) [Pubmed]
  27. Molecular modes of action of cantharidin in tumor cells. Efferth, T., Rauh, R., Kahl, S., Tomicic, M., Böchzelt, H., Tome, M.E., Briehl, M.M., Bauer, R., Kaina, B. Biochem. Pharmacol. (2005) [Pubmed]
  28. Hemoglobin scavenger receptor CD163 mediates interleukin-10 release and heme oxygenase-1 synthesis: antiinflammatory monocyte-macrophage responses in vitro, in resolving skin blisters in vivo, and after cardiopulmonary bypass surgery. Philippidis, P., Mason, J.C., Evans, B.J., Nadra, I., Taylor, K.M., Haskard, D.O., Landis, R.C. Circ. Res. (2004) [Pubmed]
  29. Pharmacokinetics of cefetamet in plasma and skin blister fluid. Zimmerli, W., Sansano, S., Wittke, B. Antimicrob. Agents Chemother. (1996) [Pubmed]
  30. Inhibition of mouse neuromuscular transmission and contractile function by okadaic acid and cantharidin. Hong, S.J. Br. J. Pharmacol. (2000) [Pubmed]
  31. Lymphangitis and refractory lymphedema after treatment with topical cantharidin. Stazzone, A.M., Borgs, P., Witte, C.L., Witte, M.H. Archives of dermatology. (1998) [Pubmed]
  32. Quantitative determination of cantharidin in biological materials using capillary gas chromatography with flame ionization detection. Carrel, J.E., Doom, J.P., McCormick, J.P. J. Chromatogr. (1985) [Pubmed]
 
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