Anisomycin activates JNK and sensitises DU 145 prostate carcinoma cells to Fas mediated apoptosis
2002

Anisomycin and Prostate Cancer Cells

publication Evidence: moderate

Author Information

Author(s): Curtin J F, Cotter T G

Primary Institution: Department of Biochemistry, University College Cork

Hypothesis

Anisomycin activates JNK and sensitizes DU 145 prostate carcinoma cells to Fas mediated apoptosis.

Conclusion

Anisomycin sensitizes DU 145 cells to Fas mediated apoptosis by activating JNK, which is essential for the apoptotic process.

Supporting Evidence

  • Anisomycin was found to stimulate prolonged JNK activation in DU 145 cells.
  • Co-treatment with anisomycin and anti-Fas IgM resulted in significant apoptosis in DU 145 cells.
  • Activation of Caspase 3 was observed when DU 145 cells were treated with both anisomycin and anti-Fas IgM.

Takeaway

This study shows that a drug called anisomycin can help make cancer cells more likely to die when treated with another substance, which could help in treating prostate cancer.

Methodology

DU 145 cells were treated with anisomycin and anti-Fas IgM, and various assays were performed to assess apoptosis and JNK activation.

Limitations

The study primarily focuses on in vitro results, which may not fully translate to in vivo conditions.

Digital Object Identifier (DOI)

10.1038/sj.bjc.6600612

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