Enhanced expression of PCAF endows apoptosis resistance in cisplatin-resistant cells

Gen Hirano, Hiroto Izumi, Akihiko Kidani, Yoshihiro Yasuniwa, Bin Han, Hitoshi Kusaba, Koichi Akashi, Michihiko Kuwano, Kimitoshi Kohno

Research output: Contribution to journalArticlepeer-review

44 Citations (Scopus)


Histone acetyltransferase (HAT) regulates transcription. We have previously shown that two HAT genes, Clock and Tip60, are overexpressed, and upregulate glutathione biosynthesis and the expression of DNA repair genes in cisplatin-resistant cells. To better understand the mechanism of HAT-related drug resistance, we investigated the role of another HAT gene, p300/CBP-associated factor (PCAF ), and found that PCAF was also overexpressed in cisplatin-resistant cells and endowed an antiapoptotic phenotype through enhanced E2F1 expression. PCAF-overexpressing cells showed enhanced expression of E2F1 and conferred cell resistance to chemotherapeutic agents. Downregulation of PCAF decreased E2F1 expression and sensitized cells to chemotherapeutic agents. Moreover, knockdown of PCAF induced G1 arrest and apoptosis. These results suggest that PCAF is one of pleiotropic factors for drug resistance and seems to be critical for cancer cell growth.

Original languageEnglish
Pages (from-to)864-872
Number of pages9
JournalMolecular Cancer Research
Issue number6
Publication statusPublished - Jun 2010

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Oncology
  • Cancer Research


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