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[Cancer Research 66, 7859-7863, August 15, 2006]
© 2006 American Association for Cancer Research

Priority Reports

Disruption of Scaffold Attachment Factor B1 Leads to TBX2 Up-regulation, Lack of p19ARF Induction, Lack of Senescence, and Cell Immortalization

Klaudia M. Dobrzycka1, Kaiyan Kang1, Shiming Jiang1, Rene Meyer1, Pulivarthi H. Rao2, Adrian V. Lee1 and Steffi Oesterreich1

1 Departments of Medicine and Molecular and Cellular Biology, The Breast Center and 2 Texas Children's Cancer Center, Baylor College of Medicine, Houston, Texas

Requests for reprints: Steffi Oesterreich, The Breast Center, Baylor College of Medicine, One Baylor Plaza, BCM 600, Houston, TX 77030. Phone: 713-798-1623; Fax: 713-798-1642; E-mail: steffio{at}breastcenter.tmc.edu.

Scaffold attachment factor B1 (SAFB1) is a multifunctional protein, which has previously been implicated in breast cancer. Here, we show that genetic deletion of SAFB1 in mouse embryonic fibroblasts (MEF) leads to spontaneous immortalization and altered expression of two proteins involved in immortalization and escape from senescence: low levels of p19ARF and high levels of TBX2. Inactivation of TBX2 using a dominant-negative TBX2 resulted in up-regulation of p19ARF in SAFB1 knockout MEFs. SAFB1 loss also caused lack of contact inhibition, increased foci formation, and increased oncogene-induced anchorage-independent growth. These findings suggest that SAFB1 is a novel player in cellular immortalization and transformation. (Cancer Res 2006; 66(16): 7859-63)




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T. L. Vormer, F. Foijer, C. L. C. Wielders, and H. te Riele
Anchorage-Independent Growth of Pocket Protein-Deficient Murine Fibroblasts Requires Bypass of G2 Arrest and Can Be Accomplished by Expression of TBX2
Mol. Cell. Biol., December 15, 2008; 28(24): 7263 - 7273.
[Abstract] [Full Text] [PDF]


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Copyright © 2006 by the American Association for Cancer Research.