Disruption of scaffold attachment factor B1 leads to TBX2 up-regulation, lack of p19ARF induction, lack of senescence, and cell immortalization

Klaudia M. Dobrzycka; Kaiyan Kang; Shiming Jiang; Rene Meyer; Pulivarthi H. Rao; Adrian V. Lee; Steffi Oesterreich

doi:10.1158/0008-5472.CAN-06-1381

Disruption of scaffold attachment factor B1 leads to TBX2 up-regulation, lack of p19^ARF induction, lack of senescence, and cell immortalization

Klaudia M. Dobrzycka, Kaiyan Kang, Shiming Jiang, Rene Meyer, Pulivarthi H. Rao, Adrian V. Lee, Steffi Oesterreich

Research output: Contribution to journal › Article › peer-review

17 Scopus citations

Abstract

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 p19^ARF and high levels of TBX2. Inactivation of TBX2 using a dominant-negative TBX2 resulted in up-regulation of p19^ARF 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.

Original language	English (US)
Pages (from-to)	7859-7863
Number of pages	5
Journal	Cancer Research
Volume	66
Issue number	16
DOIs	https://doi.org/10.1158/0008-5472.CAN-06-1381
State	Published - Aug 15 2006

ASJC Scopus subject areas

Oncology
Cancer Research

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title = "Disruption of scaffold attachment factor B1 leads to TBX2 up-regulation, lack of p19ARF induction, lack of senescence, and cell immortalization",

abstract = "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.",

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AU - Dobrzycka, Klaudia M.

AU - Kang, Kaiyan

AU - Jiang, Shiming

AU - Meyer, Rene

AU - Rao, Pulivarthi H.

AU - Lee, Adrian V.

AU - Oesterreich, Steffi

PY - 2006/8/15

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AB - 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.

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Disruption of scaffold attachment factor B1 leads to TBX2 up-regulation, lack of p19^ARF induction, lack of senescence, and cell immortalization

Abstract

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