Nfkb 1 is dispensable for Myc-induced lymphomagenesis

Ulrich Keller; Jonas A Nilsson; Kirsteen H Maclean; Jennifer B Old; John L Cleveland

doi:10.1038/sj.onc.1208779

Nfkb 1 is dispensable for Myc-induced lymphomagenesis

Ulrich Keller, Jonas A Nilsson, Kirsteen H Maclean, Jennifer B Old, John L Cleveland

UWA Centre for Medical Research (affiliated with the Harry Perkins Institute of Medical Research)

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

35 Citations (Scopus)

Abstract

Rel/NF-kappaB transcription factors are critical arbiters of immune responses, cell survival, and transformation, and are frequently deregulated in cancer. The p50 NF-kappaB 1 component of Rel/NF-kappaB DNA-binding dimers regulates genes involved in both cell cycle traverse and apoptosis. Nfkb 1 loss accelerates B cell growth and leads to increased B cell turnover in vivo, phenotypes akin to those manifested in B cells of Emu-Myc transgenic mice, a model of human Burkitt lymphoma. Interestingly, Emu-Myc B cells express reduced levels of cytoplasmic and nuclear NF-kappaB 1 and have reduced Rel/NF-kappaB DNA-binding activity, suggesting that Myc-mediated repression of NF-kappaB 1 might mediate its proliferative and apoptotic effects on B cells. Furthermore, Nfkb 1 expression was reduced in the majority of Emu-Myc lymphomas and was also suppressed in human Burkitt lymphoma. Nonetheless, loss of Nfkb 1 did not appreciably affect Myc's proliferative or apoptotic responses in B cells and had no effect on lymphoma development in Emu-Myc mice. Therefore, Nfkb 1 is dispensable for Myc-induced lymphomagenesis..

Original language	English
Pages (from-to)	6231-40
Number of pages	10
Journal	Oncogene
Volume	24
Issue number	41
DOIs	https://doi.org/10.1038/sj.onc.1208779
Publication status	Published - 15 Sept 2005

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title = "Nfkb 1 is dispensable for Myc-induced lymphomagenesis",

abstract = "Rel/NF-kappaB transcription factors are critical arbiters of immune responses, cell survival, and transformation, and are frequently deregulated in cancer. The p50 NF-kappaB 1 component of Rel/NF-kappaB DNA-binding dimers regulates genes involved in both cell cycle traverse and apoptosis. Nfkb 1 loss accelerates B cell growth and leads to increased B cell turnover in vivo, phenotypes akin to those manifested in B cells of Emu-Myc transgenic mice, a model of human Burkitt lymphoma. Interestingly, Emu-Myc B cells express reduced levels of cytoplasmic and nuclear NF-kappaB 1 and have reduced Rel/NF-kappaB DNA-binding activity, suggesting that Myc-mediated repression of NF-kappaB 1 might mediate its proliferative and apoptotic effects on B cells. Furthermore, Nfkb 1 expression was reduced in the majority of Emu-Myc lymphomas and was also suppressed in human Burkitt lymphoma. Nonetheless, loss of Nfkb 1 did not appreciably affect Myc's proliferative or apoptotic responses in B cells and had no effect on lymphoma development in Emu-Myc mice. Therefore, Nfkb 1 is dispensable for Myc-induced lymphomagenesis..",

keywords = "Animals, Base Sequence, Burkitt Lymphoma/genetics, DNA/metabolism, DNA Primers, Humans, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, NF-kappa B p50 Subunit/genetics, Proto-Oncogene Proteins c-myc/genetics",

author = "Ulrich Keller and Nilsson, {Jonas A} and Maclean, {Kirsteen H} and Old, {Jennifer B} and Cleveland, {John L}",

year = "2005",

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doi = "10.1038/sj.onc.1208779",

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journal = "Oncogene",

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T1 - Nfkb 1 is dispensable for Myc-induced lymphomagenesis

AU - Keller, Ulrich

AU - Nilsson, Jonas A

AU - Maclean, Kirsteen H

AU - Old, Jennifer B

AU - Cleveland, John L

PY - 2005/9/15

Y1 - 2005/9/15

N2 - Rel/NF-kappaB transcription factors are critical arbiters of immune responses, cell survival, and transformation, and are frequently deregulated in cancer. The p50 NF-kappaB 1 component of Rel/NF-kappaB DNA-binding dimers regulates genes involved in both cell cycle traverse and apoptosis. Nfkb 1 loss accelerates B cell growth and leads to increased B cell turnover in vivo, phenotypes akin to those manifested in B cells of Emu-Myc transgenic mice, a model of human Burkitt lymphoma. Interestingly, Emu-Myc B cells express reduced levels of cytoplasmic and nuclear NF-kappaB 1 and have reduced Rel/NF-kappaB DNA-binding activity, suggesting that Myc-mediated repression of NF-kappaB 1 might mediate its proliferative and apoptotic effects on B cells. Furthermore, Nfkb 1 expression was reduced in the majority of Emu-Myc lymphomas and was also suppressed in human Burkitt lymphoma. Nonetheless, loss of Nfkb 1 did not appreciably affect Myc's proliferative or apoptotic responses in B cells and had no effect on lymphoma development in Emu-Myc mice. Therefore, Nfkb 1 is dispensable for Myc-induced lymphomagenesis..

AB - Rel/NF-kappaB transcription factors are critical arbiters of immune responses, cell survival, and transformation, and are frequently deregulated in cancer. The p50 NF-kappaB 1 component of Rel/NF-kappaB DNA-binding dimers regulates genes involved in both cell cycle traverse and apoptosis. Nfkb 1 loss accelerates B cell growth and leads to increased B cell turnover in vivo, phenotypes akin to those manifested in B cells of Emu-Myc transgenic mice, a model of human Burkitt lymphoma. Interestingly, Emu-Myc B cells express reduced levels of cytoplasmic and nuclear NF-kappaB 1 and have reduced Rel/NF-kappaB DNA-binding activity, suggesting that Myc-mediated repression of NF-kappaB 1 might mediate its proliferative and apoptotic effects on B cells. Furthermore, Nfkb 1 expression was reduced in the majority of Emu-Myc lymphomas and was also suppressed in human Burkitt lymphoma. Nonetheless, loss of Nfkb 1 did not appreciably affect Myc's proliferative or apoptotic responses in B cells and had no effect on lymphoma development in Emu-Myc mice. Therefore, Nfkb 1 is dispensable for Myc-induced lymphomagenesis..

KW - Animals

KW - Base Sequence

KW - Burkitt Lymphoma/genetics

KW - DNA/metabolism

KW - DNA Primers

KW - Humans

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Mice, Transgenic

KW - NF-kappa B p50 Subunit/genetics

KW - Proto-Oncogene Proteins c-myc/genetics

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DO - 10.1038/sj.onc.1208779

M3 - Article

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SN - 0950-9232

VL - 24

SP - 6231

EP - 6240

JO - Oncogene

JF - Oncogene

IS - 41

ER -

Nfkb 1 is dispensable for Myc-induced lymphomagenesis

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