11
Views
29
CrossRef citations to date
0
Altmetric
Cell Growth and Development

Genetic Interaction between Rb and K-ras in the Control of Differentiation and Tumor Suppression

, , , &
Pages 10406-10415 | Received 12 Apr 2004, Accepted 02 Sep 2004, Published online: 27 Mar 2023

REFERENCES

  • Capen, C. C., Karbe E., Deschl U., George C., Germann P.-G., Gopinath C., Hardisty J. F., Kanno J., Kaufmann W., Krinke G., Kuttler K., Kulwich B., Landes C., Lenz B., Longeart L., Paulson I., Sander E., and Tuch K.. 2001. Endocrine system, p. 269–322. In Mohr U. (ed.), International classification of rodent tumors: the mouse. Springer-Verlag, Berlin, Germany.
  • Charles, A., Tang X., Crouch E., Brody J. S., and Xiao Z. X.. 2001. Retinoblastoma protein complexes with C/EBP proteins and activates C/EBP-mediated transcription. J. Cell. Biochem. 83:414–425.
  • Chen, P.-L., Riley D. J., Chen Y., and Lee W.-H.. 1996. Retinoblastoma protein positively regulates terminal adipocyte differentiation through direct interaction with C/EBPs. Genes Dev. 10:2794–2804.
  • Chen, P.-L., Riley D. J., Chen-Kiang S., and Lee W.-H.. 1996. Retinoblastoma protein directly interacts with and activates the transcription factor NF-IL6. Proc. Natl. Acad. Sci. USA 93:465–469.
  • Clarke, A. R., Maandag E. R., van Roon M., van der Lugt N. M. T., van der Valk M., Hooper M. L., Berns A., and te Riele H.. 1992. Requirement for a functional Rb-1 gene in murine development. Nature 359:328–330.
  • Classon, M., Kennedy B. K., Mulloy R., and Harlow E.. 2000. Opposing roles of pRB and p107 in adipocyte differentiation. Proc. Natl. Acad. Sci. USA 97:10826–10831.
  • de Bruin, A., Wu L., Saavedra H. I., Wilson P., Yang W., Rosol T. J., Weinstein M., Rosinson M. L., and Leone G.. 2003. Rb function in extraembryonic lineages suppresses apoptosis in CNS of Rb-deficient mice. Proc. Natl. Acad. Sci. USA 100:6546–6551.
  • Dryja, T. P., Rapaport J., McGee T. L., Nork T. M., and Schwartz T. L.. 1993. Molecular etiology of low-penetrance retinoblastoma in two pedigrees. Am. J. Genet. 52:1122–1128.
  • Dyson, N. 1998. The regulation of E2F by pRB-family proteins. Genes Dev. 12:2245–2262.
  • Goodrich, D. W., and Lee W. H.. 1993. Molecular characterization of the retinoblastoma susceptibility gene. Biochim. Biophys. Acta 1155:43–61.
  • Gu, W., Schneider J. W., Condorelli G., Kaushal S., Mahdavi V., and Nadal-Ginard B.. 1993. Interaction of myogenic factors and the retinoblastoma protein mediates muscle cell commitment and differentiation. Cell 72:309–324.
  • Hansen, J. B., Petersen R. K., Jorgensen C., and Kristiansen K.. 2002. Deregulated MAPK activity prevents adipocyte differentiation in fibroblasts lacking the retinoblastoma protein. J. Biol. Chem. 277:26335–26339.
  • Harrison, D. J., Hooper M. L., Armstrong J. F., and Clarke A. R.. 1995. Effects of heterozygosity for the Rb-1t19neo allele in the mouse. Oncogene 20:1615–1620.
  • Hu, N., Gutsmann A., Herbert D. C., Bradley A., Lee W.-H., and Lee E. Y.. 1994. Heterozygous Rb-1 delta 20/+ mice are predisposed to tumors of the pituitary gland with a nearly complete penetrance. Oncogene 9:1021–1027.
  • Jacks, T., Fazeli A., Schmitt E. M., Bronson R. T., Goodell M. A., and Weinberg R. A.. 1992. Effects of an Rb mutation in the mouse. Nature 359:295–300.
  • Johnson, L., Greenbaum D., Cichowski K., Mercer K., Murphy E., Schmitt E., Bronson R. T., Umanoff H., Windfried E., Kucherlapati R., and Jacks T.. 1997. K-ras is an essential gene in the mouse with partial functional overlap with N-ras. Genes Dev. 11:2468–2481.
  • Jones, M. K., and Jackson J. H.. 1998. Ras-GRF activates Ha-Ras, but not N-Ras or K-Ras 4B, protein in vivo. J. Biol. Chem. 273:1782–1787.
  • Koera, K., Nakamura K., Nakao K., Miyoshi J., Toyoshima K., Hatta T., Otani H., Aiba A., and Katsuki M.. 1997. K-Ras is essential for the development of the mouse embryo. Oncogene 15:1151–1159.
  • Kratzke, R. A., Otterson G. A., Hogg A., Coxon A. B., Geradts J., Cowell J. K., and Kaye F. J.. 1994. Partial inactivation of RB product in a family with incomplete penetrance of familial retinoblastoma and benign retinal tumors. Oncogene 9:1321–1326.
  • Lasorella, A., Noseda M., Beyna M., and Iavarone A.. 2000. Id2 is a retinoblastoma protein target and mediates signalling by Myc oncoproteins. Nature 407:592–598.
  • Lee, E. Y.-H. P., Chang C.-Y., Hu N., Wang Y.-C. J., Lai C.-C., Herrup K., Lee W.-H., and Bradley A.. 1992. Mice deficient for Rb are nonviable and show defects in neurogenesis and haematopoiesis. Nature 359:288–294.
  • Lee, K. Y., Ladha M. H., McMahon C., and Ewen M. E.. 1999. The retinoblastoma protein is linked to the activation of Ras. Mol. Cell. Biol. 19:7724–7732.
  • Leone, G., DeGregori J., Sears R., Jakoi L., and Nevins J. R.. 1997. Myc and Ras collaborate in inducing accumulation of active cyclin E/Cdk2 and E2F. Nature 387:422–426.
  • Lohmann, D. R., Brandt B., Hopping W., Passarge E., and Horsthemke B.. 1994. Distinct RB1 gene mutations with low penetrance in hereditary retinoblastoma. Hum. Genet. 94:349–354.
  • MacPherson, D., Sage J., Crowley D., Trumpp A., Bronson R. T., and Jacks T.. 2003. Conditional mutation of Rb causes cell cycle defects without apoptosis in the central nervous system. Mol. Cell. Biol. 23:1044–1053.
  • Mittnacht, S., Paterson H., Olson M. F., and Marshall C. J.. 1997. Ras signalling is required for inactivation of tumour suppressor pRb cell-cycle control protein. Curr. Biol. 7:219–221.
  • Novitch, B. G., Mulligan G. J., Jacks T., and Lassar A. B.. 1996. Skeletal muscle cells lacking the retinoblastoma protein display defects in muscle gene expression and accumulate in S and G2 phases of the cell cycle. J. Cell Biol. 135:441–456.
  • Novitch, B. G., Spicer D. B., Kim P. S., Cheung W. L., and Lassar A. B.. 1999. pRb is required for MEF2-dependent gene expression as well as cell-cycle arrest during skeletal muscle differentiation. Curr. Biol. 9:449–459.
  • Onadim, Z., Hogg A., Baird P. N., and Cowell J. K.. 1992. Oncogenic point mutations in exon 20 of the RB1 gene in families showing incomplete penetrance and mild expression of the retinoblastoma phenotype. Proc. Natl. Acad. Sci. USA 89:6177–6181.
  • Peeper, D. S., Upton T. M., Ladha M. H., Neuman E., Zalvide J., Bernards R., DeCaprio J. A., and Ewen M. E.. 1997. Ras signalling linked to the cell-cycle machinery by the retinoblastoma protein. Nature 386:177–181.
  • Raptis, L., Brownell H. L., Corbley M. J., Wood K. W., Wang D., and Haliotis T.. 1997. Cellular ras gene activity is required for full neoplastic transformation by the large tumor antigen of SV40. Cell Growth Differ. 8:891–901.
  • Riley, D. J., Nikitin A. Y., and Lee W.-H.. 1996. Adenovirus-mediated retinoblastoma gene therapy suppresses spontaneous pituitary melanotroph tumors in Rb+/− mice. Nat. Med. 2:1316–1321.
  • Saavendra, H. I., Wu L., de Bruin A., Timmers C., Rosol T. J., Weinstein M., Robinson M. L., and Leone G.. 2002. Specificity of E2F1, E2F2 and E2F3 in mediating phenotypes induced by loss of Rb. Cell Growth Differ. 13:215–225.
  • Sellers, W. R., Novitch B. G., Miyake S., Heith A., Otterson G. A., Kaye F. J., Lassar A. B., and Kaelin W. G. J.. 1998. Stable binding to E2F is not required for the retinoblastoma protein to activate transcription, promote differentiation, and suppress tumor growth. Genes Dev. 12:96–106.
  • Singh, P., Chan S. W., and Hong W.. 2001. Retinoblastoma protein is functionally distinct from its homologues in affecting glucocorticoid receptor-mediated transcription and apoptosis. J. Biol. Chem. 276:13762–13770.
  • Singh, P., Coe J., and Hong W.. 1995. A role for the retinoblastoma protein in potentiating transcriptional activation of the glucocorticoid receptor. Nature 374:562–565.
  • Takahashi, C., Akiyama N., Matsuzaki T., Takai S., Kitayama H., and Noda M.. 1996. Characterization of a human MSX-2 cDNA and its fragment isolated as a transformation suppressor gene against v-Ki-ras oncogene. Oncogene 12:2137–2146.
  • Takahashi, C., Bronson R. T., Socolovsky M., Contreras B., Lee K. Y., Jacks T., Noda M., Kucherlapati R., and Ewen M. E.. 2003. Rb and N-ras function together to control differentiation in the mouse. Mol. Cell. Biol. 23:5256–5268.
  • Tenen, D. G. 2003. Disruption of differentiation in human cancer: AML shows the way. Nat. Rev. Cancer 3:89–101.
  • Thomas, D. M., Carty S. A., Piscopo D. M., Lee J.-S., Wang W.-F., Forrester W. C., and Hinds P. W.. 2001. The retinoblastoma protein acts as a transcriptional coactivator required for osteogenic differentiation. Mol. Cell 8:303–316.
  • Tsai, K. Y., Hu Y., Macleod K. F., Crowley D., Yamasaki L., and Jacks T.. 1998. Mutation of E2f-1 suppresses apoptosis and inappropriate S phase entry and extends survival of Rb-deficient mouse embryos. Mol. Cell 2:293–304.
  • Whitaker, L. L., Su H., Baskaran R., Knudsen E. S., and Wang J. Y. J.. 1998. Growth suppression by an E2F-binding-defective retinoblastoma protein (RB): contribution from the RB C pocket. Mol. Cell. Biol. 18:4032–4042.
  • White, A., and Gibson S.. 1998. ACTH precursors: biological significance and clinical relevance. Clin. Endocrinol. (Oxford) 48:251–255.
  • Williams, B. O., Remington L., Albert D. M., Mukai S., Bronson R. T., and Jacks T.. 1994. Cooperative tumorigenic effects of germline mutations in Rb and p53. Nat. Genet. 7:480–484.
  • Wu, L., de Bruin A., Saavedra H. I., Starovic M., Trimboli A., Yang Y., Opavska J., Wilson P., Thompson J. C., Ostrowski M. C., Rosol T. J., Woollett L. A., Weinstein M., Cross J. C., Rosinson M. L., and Leone G.. 2003. Extra-embryonic function of Rb is essential for embryonic development and viability. Nature 421:942–947.
  • Yamasaki, L., Bronson R., Williams B. O., Dyson N. J., Harlow E., and Jacks T.. 1998. Loss of E2F-1 reduces tumorigenesis and extends the lifespan of Rb1+/− mice. Nat. Genet. 18:360–364.
  • Zacksenhaus, E., Jiang Z., Chung D., Marth J. D., Phillips R. A., and Gallie B. L.. 1996. pRb controls proliferation, differentiation, and death of skeletal muscle cells and other lineages during embryogenesis. Genes Dev. 10:3051–3064.
  • Ziebold, U., Lee E. Y., Bronson R. T., and Lees J. A.. 2003. E2F3 loss has opposite effects on different pRB-deficient tumors, resulting in suppression of pituitary tumors but metastasis of medullary thyroid carcinomas. Mol. Cell. Biol. 23:6542–6552.
  • Ziebold, U., Reza T., Caron A., and Lees J. A.. 2001. E2F3 contributes both to the inappropriate proliferation and to the apoptosis arising in Rb mutant embryos. Genes Dev. 15:386–391.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.