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The effects of chelidonine on tubulin polymerisation, cell cycle progression and selected signal transmission pathways

  1. Author:
    Panzer, A.
    Joubert, A. M.
    Bianchi, P. C.
    Hamel, E.
    Seegers, J. C.

  2. Author Address

    Univ Pretoria, Dept Physiol, POB 2034, ZA-0001 Pretoria, South Africa. Univ Pretoria, Dept Physiol, ZA-0001 Pretoria, South Africa. Univ Witwatersrand, Dept Surg, Witwatersrand, South Africa. NCI, Lab Drug Discovery Res & Dev, Dev Therapeut Program, Div Canc Treatment & Diag, Frederick Canc Res & Dev Ctr, Frederick, MD 21701 USA. Joubert AM Univ Pretoria, Dept Physiol, POB 2034, ZA-0001 Pretoria, South Africa.
    1. Year: 2001
  2. Journal: European Journal of Cell Biology
    1. 80
    2. 1
    3. Pages: 111-118
  4. Type of Article: Article
  1. Abstract:

    Chelidonine is a tertiary benzophenanthridine alkaloid known to cause mitotic arrest and to interact weakly with tubulin. Our interest in chelidonine began when we found it to be a major contaminant of Ukrain(TM), which is a compound reported to be selectively toxic to malignant tells. The effects of chelidonine in two normal (monkey kidney and Hs27), two transformed (Vero and Graham 293) and two malignant (WHCO5 and HeLa) cell lines, were examined. Chelidonine proved to be a weak inhibitor of cell growth, but no evidence for selective cytotoxicity was found in this study. It was confirmed that chelidonine inhibits tubulin polymerisation (IC50 = 24 muM), explaining its ability to disrupt microtubular structure in cells. A G2/M arrest results, which is characterised by abnormal metaphase morphology, increased levels of cyclin B1 and enhanced cdc2 kinase activity. Exposure of all cell lines examined to chelidonine leads to activation of the stress- activated protein kinase/jun kinase pathway (SAPK/JNK).

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