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Cited by 1,065

The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.

Bmi-1 collaborates with c-Myc in tumorigenesis by inhibiting c-Myc-induced apoptosis via INK4a/ARF

Open access
Jacobs, J. J.L., Scheijen, B., Voncken, J.-W., Kieboom, K., Berns, A., van Lohuizen, M.·1999·Genes & Development
DOI 10.1101/gad.13.20.2678
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Abstract

The bmi-1 and myc oncogenes collaborate strongly in murine lymphomagenesis, but the basis for this collaboration was not understood. We recently identified the ink4a-ARF tumor suppressor locus as a critical downstream target of the Polycomb-group transcriptional repressor Bmi-1. Others have shown that part of Myc's ability to induce apoptosis depends on induction of p19arf. Here we demonstrate that down-regulation of ink4a-ARF by Bmi-1 underlies its ability to cooperate with Myc in tumorigenesis. Heterozygosity for bmi-1 inhibits lymphomagenesis in Emu-myc mice by enhancing c-Myc-induced apoptosis. We observe increased apoptosis in bmi-1(-/-) lymphoid organs, which can be rescued by deletion of ink4a-ARF or overexpression of bcl2. Furthermore, Bmi-1 collaborates with Myc in enhancing proliferation and transformation of primary embryo fibroblasts (MEFs) in an ink4a-ARF dependent manner, by prohibiting Myc-mediated induction of p19arf and apoptosis. We observe strong collaboration between the Emu-myc transgene and heterozygosity for ink4a-ARF, which is accompanied by loss of the wild-type ink4a-ARF allele and formation of highly aggressive B-cell lymphomas. Together, these results reinforce the critical role of Bmi-1 as a dose-dependent regulator of ink4a-ARF, which on its turn acts to prevent tumorigenesis on activation of oncogenes such as c-myc.

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Metadata

Authors
Jacobs, J. J. L., Scheijen, B., Voncken, J.-W., Kieboom, K., Berns, A., & van Lohuizen, M.
Venue
Genes & Development
Publisher
Cold Spring Harbor Laboratory
Published
1999-10-15
Volume
13
Issue
20
Pages
2678-2690
ISSN
0890-9369 (ISSN-L)
DOI
10.1101/gad.13.20.2678
OpenAlex
W2105298978
Cited by
1,065
References
15
Type
posted content
Language
en
Open access
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