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Molecular Cancer
Published in: Molecular Cancer 1/2006

Open Access 01-12-2006 | Research

Myb proteins inhibit fibroblast transformation by v-Rel

Published in: Molecular Cancer | Issue 1/2006

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Abstract

Genes that cause cancer have been divided into two general classes – oncogenes that act in a dominant fashion to transform normal cells into a malignant state, and tumor suppressor genes that act in a dominant fashion to prevent such transformation. In this report, we demonstrate that both the v-myb retroviral oncogene, which causes leukemic transformation of hematopoietic cells, and the c-myb proto-oncogene can also function as inhibitors of fibroblast transformation by the v-rel oncogene. These results imply that the myb genes can function either as oncogenes or as tumor suppressors in different cellular contexts.
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Literature
1.
Hahn WC, Weinberg RA: Modelling the molecular circuitry of cancer. Nat Rev Cancer. 2002, 2: 331-341. 10.1038/nrc795CrossRefPubMed
2.
Lipsick JS, Wang DM: Transformation by v-Myb. Oncogene. 1999, 18: 3047-3055. 10.1038/sj.onc.1202745CrossRefPubMed
3.
4.
McNagny KM, Graf T: Acute avian leukemia viruses as tools to study hematopoietic cell differentiation. CurrTopMicrobiolImmunol. 1996, 212: 143-162.
5.
Leprince D, Gegonne A, Coll J, de Taisne C, Schneeberger A, Lagrou C, Stehelin D: A putative second cell-derived oncogene of the avian leukaemia retrovirus E26. Nature. 1983, 306: 395-397. 10.1038/306395a0CrossRefPubMed
6.
Gilmore TD: The Re1/NF-kappa B/I kappa B signal transduction pathway and cancer. Cancer Treat Res. 2003, 115: 241-265.CrossRefPubMed
7.
Moore BE, Bose HR: Expression of the v-rel oncogene in reticuloendotheliosis virus-transformed fibroblasts. Virology. 1988, 162: 377-387. 10.1016/0042-6822(88)90478-3CrossRefPubMed
8.
Aggarwal BB: Nuclear factor-kappaB: the enemy within. Cancer Cell. 2004, 6: 203-208. 10.1016/j.ccr.2004.09.003CrossRefPubMed
9.
Jang SK, Davies MV, Kaufman RJ, Wimmer E: Initiation of protein synthesis by internal entry of ribosomes into the 5' nontranslated region of encephalomyocarditis virus RNA in vivo. Journal of Virology. 1989, 63: 1651-1660.PubMedCentralPubMed
10.
Ghattas IR, Sanes JR, Majors JE: The encephalomyocarditis virus internal ribosome entry site allows efficient coexpression of two genes from a recombinant provirus in cultured cells and in embryos. Molecular and Cellular Biology. 1991, 11: 5848-5859.PubMedCentralPubMed
11.
Lipsick JS, Ibanez CE, Baluda MA: Expression of molecular clones of v-myb in avian and mammalian cells independently of transformation. J Virol. 1986, 59: 267-275.PubMedCentralPubMed
12.
Perbal B, Lipsick JS, Svoboda J, Silva RF, Baluda MA: Biologically active proviral clone of myeloblastosis-associated virus type 1: Implications for the genesis of avian myeloblastosis virus. Journal of Virology. 1985, 56: 240-244.PubMedCentralPubMed
13.
Boehmelt G, Walker A, Kabrun N, Mellitzer G, Beug H, Zenke M, Enrietto PJ: Hormone-regulated v-rel estrogen receptor fusion protein: reversible induction of cell transformation and cellular gene expression. EMBO Journal. 1992, 11: 4641-4652.PubMedCentralPubMed
14.
Baluda MA, Reddy EP: Anatomy of an integrated avian myeloblastosis provirus: structure and function. Oncogene. 1994, 9: 2761-2774.PubMed
15.
Ferrao P, Macmillan EM, Ashman LK, Gonda TJ: Enforced expression of full length c-Myb leads to density-dependent transformation of murine haemopoietic cells. Oncogene. 1995, 11: 1631-1638.PubMed
16.
Fu SL, Lipsick JS: Constitutive expression of full-length c-Myb transforms avian cells characteristic of both the monocytic and granulocytic lineages. Cell Growth Differ. 1997, 8: 35-45.PubMed
17.
Morrison LE, Boehmelt G, Beug H, Enrietto PJ: Expression of v-rel in a replication competent virus: transformation and biochemical characterization. Oncogene. 1991, 6: 1657-1666.PubMed
18.
Richardson PM, Gilmore TD: vRel is an inactive member of the Rel family of transcriptional activating proteins. J Virol. 1991, 65: 3122-3130.PubMedCentralPubMed
19.
Sarkar S, Gilmore TD: Transformation by the vRel oncoprotein requires sequences carboxy-terminal to the Rel homology domain. Oncogene. 1993, 8: 2245-2252.PubMed
20.
Gill G, Ptashne M: Negative effect of the transcriptional activator GAL4. Nature. 1988, 334: 721-724. 10.1038/334721a0CrossRefPubMed
21.
Joaquin M, Watson RJ: Cell cycle regulation by the B-Myb transcription factor. Cell Mol Life Sci. 2003, 60: 2389-2401. 10.1007/s00018-003-3037-4CrossRefPubMed
22.
Neiman PE, Grbic JJ, Polony TS, Kimmel R, Bowers SJ, Delrow J, Beemon KL: Functional genomic analysis reveals distinct neoplastic phenotypes associated with c-myb mutation in the bursa of Fabricius. Oncogene. 2003, 22: 1073-1086. 10.1038/sj.onc.1206070CrossRefPubMed
23.
Guerin M, Sheng ZM, Andrieu N, Riou G: Strong association between c-myb and oestrogen-receptor expression in human breast cancer. Oncogene. 1990, 5: 131-135.PubMed
24.
Dini PW, Lipsick JS: Oncogenic truncation of the first repeat of c-Myb decreases DNA binding in vitro and in vivo. Mol Cell Biol. 1993, 13: 7334-7348.PubMedCentralPubMed
25.
Grasser FA, LaMontagne K, Whittaker L, Stohr S, Lipsick JS: A highly conserved cysteine in the v-Myb DNA-binding domain is essential for transformation and transcriptional trans-activation. Oncogene. 1992, 7: 1005-1009.PubMed
26.
Dini PW, Eltman JT, Lipsick JS: Mutations in the DNA-binding and transcriptional activation domains of v-Myb cooperate in transformation. J Virol. 1995, 69: 2515-2524.PubMedCentralPubMed
27.
28.
Evan GI, Lewis GK, Bishop JM: Isolation of monoclonal antibodies specific for products of avian oncogene myb. Mol Cell Biol. 1984, 4: 2843-2850.PubMedCentralPubMed
29.
Harlow E, Lane DP: Antibodies: A laboratory manual. 1988, Cold Spring Harbor, Cold Spring Harbor Laboratory.
30.
Sleeman JP: Xenopus A-myb is expressed during early spermatogenesis. Oncogene. 1993, 8: 1931-1941.PubMed
Metadata
Title
Myb proteins inhibit fibroblast transformation by v-Rel
Publication date
01-12-2006
Published in
Molecular Cancer / Issue 1/2006
Electronic ISSN: 1476-4598
DOI
https://doi.org/10.1186/1476-4598-5-54

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