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A more recent version of this article appeared on December 23, 2005
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M508270200v1
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Papers In Press, published online ahead of print October 26, 2005
J. Biol. Chem, 10.1074/jbc.M508270200
Submitted on July 28, 2005
Revised on September 20, 2005
Accepted on October 26, 2005

Regulation of the INK4A/ARF locus by HDAC inhibitors

Ander Matheu, Peter Klatt, and Manuel Serrano

Molecular Oncology, Spanish National Cancer Center (CNIO), Madrid 28029

Corresponding Author: mserrano{at}cnio.es

Despite the importance of the INK4a/ARF locus in tumor suppression, its modulation by histone deacetylase inhibitors (HDACis) remains to be characterized. Here, we show that the levels of p16INK4a are decreased in human and murine fibroblasts upon exposure to relatively high concentrations of trichostatin A (TSA) and sodium butyrate (NaB). Interestingly, in contrast to p16INK4a, the levels of p19ARF are strongly upregulated in murine cells even at low concentrations of HDACis. Using ARF-deficient cells, we demonstrate that p19ARF plays an active role in HDACi-triggered cytostasis, and the contribution of p19ARF to this arrest is of comparatively higher magnitude than that of the well-established HDACi target p21Waf1/Cip. Moreover, chemically-induced fibrosarcomas in ARF-null mice are more resistant to the therapeutic effect of HDACis than similar tumors in wild type or p21Waf1/Cip-null mice. Together, our results establish the tumor suppressor ARF as a relevant target for HDACi chemotherapy.


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