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Taxol inhibits opioid binding on T47D human breast cancer cells.

Abstract
In the T47D human breast cancer cell line, Taxol was found to compete for ethylketocyclazocine opioid binding (IC50 3.3 pM). In contrast, no interaction of the drug with [3H]diprenorphine binding occurred. Binding was multiphasic, in the absence of colchicine (10[-6] M), but monophasic in its presence, indicating an involvement of the cytoskeleton in this process. Alignment of Taxol binding domains on alpha and beta tubulin with the kappa opioid site revealed homology of these sites with the first extracellular loop of the receptor. These results indicate a possible new action of Taxol, indicating for the first time a membrane action of the agent.
AuthorsE Bakogeorgou, A Hatzoglou, E Castanas
JournalBiochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 235 Issue 1 Pg. 201-4 (Jun 09 1997) ISSN: 0006-291X [Print] United States
PMID9196063 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Analgesics, Opioid
  • Antineoplastic Agents, Phytogenic
  • Receptors, Opioid
  • Receptors, Opioid, kappa
  • Tubulin
  • Diprenorphine
  • Ethylketocyclazocine
  • Paclitaxel
Topics
  • Amino Acid Sequence
  • Analgesics, Opioid (metabolism)
  • Antineoplastic Agents, Phytogenic (metabolism, pharmacology)
  • Binding Sites (drug effects)
  • Binding, Competitive
  • Breast Neoplasms (metabolism)
  • Diprenorphine (metabolism)
  • Ethylketocyclazocine (metabolism)
  • Humans
  • Molecular Sequence Data
  • Paclitaxel (metabolism, pharmacology)
  • Receptors, Opioid (metabolism)
  • Receptors, Opioid, kappa (metabolism)
  • Sequence Alignment
  • Tubulin (chemistry)
  • Tumor Cells, Cultured

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