JCI table of contents -- Februa...( mediated apoptosis and caused HIPK2 to ...)

mediated apoptosis and caused HIPK2 to relocate from the cell nucleus to the cytoplasm. Further, expression of HIPK2 was required for HMGA1 to inhibit p53-mediated apoptosis. Importantly, analysis of human breast cancer samples indicated that overexpression of HMGA1 correlated with the presence of HIPK2 in the cytoplasm and low levels of apoptotic cells, even in the presence of normal p53. This study therefore identifies a new mechanism by which p53-mediated apoptosis can be inhibited, leading to the development of cancer.

TITLE: High-mobility group A1 inhibits p53 by cytoplasmic relocalization of its proapoptotic activator HIPK2

AUTHOR CONTACT:
Silvia Soddu
Istituto Nazionale dei Tumori Regina Elena, Rome, Italy.
Phone: +39-065266-2563; Fax: +39-065266-2505; E-mail: soddu@ifo.it.

View the PDF of this article at: https://www.the-jci.org/article.php?id=29852

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ONCOLOGY: To be benign or malignant: mTOR makes the decision

Tuberous sclerosis complex (TSC) is a genetic disorder that results in sufferers developing benign tumors in many parts of their body. It is caused by genetic mutation of either of two genes, TSC1 or TSC2. The proteins encoded by these genes are negative regulators of a signaling pathway that is initiated at the cell surface by a ligand binding to PDGFR and that involves activation of PI3K, AKT, and mTOR. The fact that individuals with TSC develop only benign tumors is somewhat surprising because genetic mutations that cause increased PDGFR, PI3K, and AKT activity are associated with malignant cancer, as are inactivating genetic mutations of other negative regulators of this signaling pathways (including PTEN). In a study appearing online on February 8 in advance of publication in the March print issue of the Journal of Clinical Investigation, researchers from the Chinese Aca
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Contact: Karen Honey
press_releases@the-jci.org
212-342-4159
Journal of Clinical Investigation
8-Feb-2007

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