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Nucleic Acids Research Advance Access originally published online on February 17, 2009
Nucleic Acids Research 2009 37(7):2070-2086; doi:10.1093/nar/gkp067
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Nucleic Acids Research, 2009, Vol. 37, No. 7 2070-2086
© 2009 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gene Regulation, Chromatin and Epigenetics

HMGB1 and HMGB2 proteins up-regulate cellular expression of human topoisomerase II{alpha}

Michal Stros1,*, Eva Polanská1, Sona Struncová2 and Sárka Pospísilová2

1Laboratory of Analysis of Chromosomal Proteins, Academy of Sciences of the Czech Republic, Institute of Biophysics, Brno and 2Center of Molecular Biology and Gene Therapy, Department of Internal Medicine-Hematooncology, University Hospital and Medical Faculty MU Brno, Czech Republic

*To whom correspondence should be addressed. Tel: +420 541 517 183; Fax: +420 541 211 293; Email: stros{at}ibp.cz

Received August 25, 2008. Revised January 12, 2009. Accepted January 22, 2009.

Topoisomerase II{alpha} (topo II{alpha}) is a nuclear enzyme involved in several critical processes, including chromosome replication, segregation and recombination. Previously we have shown that chromosomal protein HMGB1 interacts with topo II{alpha}, and stimulates its catalytic activity. Here we show the effect of HMGB1 on the activity of the human topo II{alpha} gene promoter in different cell lines. We demonstrate that HMGB1, but not a mutant of HMGB1 incapable of DNA bending, up-regulates the activity of the topo II{alpha} promoter in human cells that lack functional retinoblastoma protein pRb. Transient over-expression of pRb in pRb-negative Saos-2 cells inhibits the ability of HMGB1 to activate the topo II{alpha} promoter. The involvement of HMGB1 and its close relative, HMGB2, in modulation of activity of the topo II{alpha} gene is further supported by knock-down of HMGB1/2, as evidenced by significantly decreased levels of topo II{alpha} mRNA and protein. Our experiments suggest a mechanism of up-regulation of cellular expression of topo II{alpha} by HMGB1/2 in pRb-negative cells by modulation of binding of transcription factor NF-Y to the topo II{alpha} promoter, and the results are discussed in the framework of previously observed pRb-inactivation, and increased levels of HMGB1/2 and topo II{alpha} in tumors.


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