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p300 mediates cellular resistance to doxorubicin in bladder cancer

Ario Takeuchi1, Masaki Shiota, Katsunori Tatsugami

  • 1Department of Urology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.

Molecular Medicine Reports
|September 22, 2011
PubMed

Insights

Reduced p300 expression in bladder cancer cells contributes to doxorubicin resistance. Targeting p300 may enhance chemotherapy effectiveness for bladder cancer patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Bladder cancer is a common malignancy with high recurrence rates after initial treatment.
  • Doxorubicin is a standard chemotherapy for advanced bladder cancer, but resistance is a significant clinical challenge.
  • Previous research implicated p300/CBP-associated factor in doxorubicin resistance, but the role of p300 itself was unknown.

Purpose of the Study:

  • To investigate the role of the histone acetyltransferase p300 in doxorubicin resistance in bladder cancer.
  • To elucidate the molecular mechanisms underlying p300's involvement in chemotherapy resistance.

Main Methods:

  • Comparative analysis of p300 expression in doxorubicin-sensitive and doxorubicin-resistant bladder cancer cell lines.
  • Assessment of p300 expression levels following doxorubicin exposure.
  • Experimental manipulation of p300 expression to evaluate its impact on doxorubicin sensitivity.

Main Results:

  • p300 expression was found to be significantly reduced in doxorubicin-resistant bladder cancer cells.
  • Doxorubicin treatment led to a decrease in p300 expression.
  • Suppression of p300 expression in bladder cancer cells induced resistance to doxorubicin.

Conclusions:

  • The histone acetyltransferase p300 plays a crucial role in modulating bladder cancer cell sensitivity to doxorubicin.
  • Reduced p300 expression is associated with doxorubicin resistance.
  • p300 represents a potential molecular therapeutic target for overcoming doxorubicin resistance in bladder cancer.

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