Maspin increases Ku70 acetylation and Bax-mediated cell death in cancer cells

  • Authors:
    • Sook-Ja Lee
    • Haerim Jang
    • Chaehwa Park
  • View Affiliations

  • Published online on: November 10, 2011     https://doi.org/10.3892/ijmm.2011.833
  • Pages: 225-230
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Abstract

Ku70, a DNA repair protein, was recently identified as a critical anti-apoptotic protein that inhibits Bax translocation to mitochondria. The dissociation of Bax from Ku70 is essential for the apoptotic activity of Bax. Here, we show that maspin, a tumor suppressor protein frequently lost in cancer, regulates this process. Maspin increased cell death in a Ku70 acetylation-dependent manner. Maspin inhibited histone deacetylase 1 (HDAC1) and thus increased the acetylation of Ku70 and the dissociation of Bax from Ku70, which led to the induction of apoptosis. These results reveal maspin as a Ku70-interacting molecule and provide the basis for a new endogenous acetylation-based control mechanism that reduces Ku70-mediated sequestration of Bax from mitochondria.

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February 2012
Volume 29 Issue 2

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Lee S, Jang H and Park C: Maspin increases Ku70 acetylation and Bax-mediated cell death in cancer cells. Int J Mol Med 29: 225-230, 2012.
APA
Lee, S., Jang, H., & Park, C. (2012). Maspin increases Ku70 acetylation and Bax-mediated cell death in cancer cells. International Journal of Molecular Medicine, 29, 225-230. https://doi.org/10.3892/ijmm.2011.833
MLA
Lee, S., Jang, H., Park, C."Maspin increases Ku70 acetylation and Bax-mediated cell death in cancer cells". International Journal of Molecular Medicine 29.2 (2012): 225-230.
Chicago
Lee, S., Jang, H., Park, C."Maspin increases Ku70 acetylation and Bax-mediated cell death in cancer cells". International Journal of Molecular Medicine 29, no. 2 (2012): 225-230. https://doi.org/10.3892/ijmm.2011.833