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Related Experiment Videos

Multiple drug resistance and intermediate filaments

A E Cress1, W S Dalton

  • 1Department of Radiation Oncology, Arizona Cancer Center, University of Arizona, Tucson 85724, USA.

Cancer Metastasis Reviews
|December 1, 1996
PubMed
Summary

Epithelial tumors exhibit intrinsic drug resistance due to cytokeratin 8 and 18 expression, a phenomenon termed cytokeratin-dependent multidrug resistance (C-MDR). This resistance is independent of cytokeratin

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Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Epithelial-derived tumors (e.g., breast, prostate) often display multidrug resistance (MDR), hindering treatment success.
  • Epithelial cells intrinsically resist chemotherapeutic agents more than hematopoietic cells, even without prior exposure.
  • Cytokeratin proteins, specifically cytokeratin 8 and 18, are characteristic of epithelial cells and tumors.

Purpose of the Study:

  • To investigate the role of cytokeratin 8 and 18 in the intrinsic drug resistance of epithelial tumors.
  • To determine if the structural assembly of cytokeratins into intermediate filaments is necessary for this drug resistance.

Main Methods:

  • Engineered cell lines expressing cytokeratin 8 and 18 were utilized to study cytokeratin-dependent multidrug resistance (C-MDR).
  • Experiments involved transfecting cells to prevent cytokeratin network formation and assessing their sensitivity to chemotherapeutic agents.

Main Results:

  • C-MDR was observed in engineered cell lines expressing cytokeratin 8 and 18.
  • Cells unable to form cytokeratin intermediate filament networks still exhibited C-MDR, indicating network formation is not required.
  • Disrupting cytokeratin network assembly did not increase tumor cell sensitivity to chemotherapeutic agents.

Conclusions:

  • The intrinsic drug resistance in epithelial tumors (C-MDR) is linked to cytokeratin 8 and 18 expression.
  • C-MDR is independent of the structural ability of cytokeratins to form intermediate filament networks.
  • A potential mechanism involves direct interaction between chemotherapeutic agents and cytokeratins, triggering cell survival signaling.

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