p300 mediates cellular resistance to doxorubicin in bladder cancer

Ario Takeuchi, Masaki Shiota, Katsunori Tatsugami, Akira Yokomizo, Shingo Tanaka, Kentaro Kuroiwa, Masatoshi Eto, Seiji Naito

Research output: Contribution to journalArticlepeer-review

26 Citations (Scopus)


Bladder cancer is one of the most common urogenital malignancies. At the non-invasive stage, bladder cancer can be completely resected transurethrally. However, 70% of patients experience intravesical tumor recurrence within 5 years. Patients with advanced bladder cancer frequently receive a chemotherapy regimen containing doxorubicin. However, doxorubicin resistance is a major obstacle to cancer chemotherapy. Previously, we reported that the histone acetyltransferase p300/CBP-associated factor is involved in doxorubicin resistance in bladder cancer. However, the role of another histone acetyltransferase, p300, in bladder cancer resistance to doxorubicin remains unclear. In this study, we investigated the molecular mechanism of doxorubicin resistance in bladder cancer with regard to p300. The result showed that p300 expression was reduced in doxorubicin-resistant bladder cancer cells and in response to doxorubicin exposure. Furthermore, p300 suppression rendered bladder cancer cells resistant to doxorubicin. Taken together, the results from this study indicate that p300 may be a promising molecular therapeutic target through the modulation of cellular sensitivity to doxorubicin in bladder cancer.

Original languageEnglish
Pages (from-to)173-176
Number of pages4
JournalMolecular medicine reports
Issue number1
Publication statusPublished - Jan 2012

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Medicine
  • Molecular Biology
  • Genetics
  • Oncology
  • Cancer Research


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