Surprising Dependency for Retinoblastoma Protein in Ras-Mediated Tumorigenesis

REFERENCES

• Bautista, D., J. R. Emanuel, C. Granville, R. Howard, and J. Costa. 1996. Identification of mutations in the Ki-ras gene in human retinoblastoma. Invest. Ophthalmol. Vis. Sci. 37:2313–2317.
   PubMedGoogle Scholar
• Berns, E. M., A. de Klein, W. L. van Putten, I. L. van Staveren, A. Bootsma, J. G. Klijn, and J. A. Foekens. 1995. Association between RB-1 gene alterations and factors of favourable prognosis in human breast cancer, without effect on survival. Int. J. Cancer 64:140–145.
   PubMedGoogle Scholar
• Borg, A., Q. X. Zhang, P. Alm, H. Olsson, and G. Sellberg. 1992. The retinoblastoma gene in breast cancer: allele loss is not correlated with loss of gene protein expression. Cancer Res. 52:2991–2994.
   PubMed Web of Science ®Google Scholar
• Bunn, P. A., Jr., and W. Franklin. 2002. Epidermal growth factor receptor expression, signal pathway, and inhibitors in non-small cell lung cancer. Semin. Oncol. 29:38–44.
   PubMed Web of Science ®Google Scholar
• Classon, M., and E. Harlow. 2002. The retinoblastoma tumour suppressor in development and cancer. Nat. Rev. Cancer 2:910–917.
   PubMed Web of Science ®Google Scholar
• Classon, M., B. K. Kennedy, R. Mulloy, and E. Harlow. 2000. Opposing roles of pRB and p107 in adipocyte differentiation. Proc. Natl. Acad. Sci. USA 97:10826–10831.
   PubMed Web of Science ®Google Scholar
• D'Abaco, G. M., S. Hooper, H. Paterson, and C. J. Marshall. 2002. Loss of Rb overrides the requirement for ERK activity for cell proliferation. J. Cell Sci. 115:4607–4616.
   PubMedGoogle Scholar
• DeGregori, J. 2002. The genetics of the E2F family of transcription factors: shared functions and unique roles. Biochim. Biophys. Acta 1602:131–150.
   PubMed Web of Science ®Google Scholar
• Enomoto, T., M. Fujita, M. Inoue, A. Nakazawa-Miyamoto, O. Tanizawa, and T. Nomura. 1993. Alterations of the Rb gene and its association with Ki-ras activation and p53 inactivation in endometrial adenocarcinoma. Mol. Carcinog. 8:132–137.
   PubMedGoogle Scholar
• Gope, R., and M. L. Gope. 1992. Abundance and state of phosphorylation of the retinoblastoma susceptibility gene product in human colon cancer. Mol. Cell. Biochem. 110:123–133.
   PubMedGoogle Scholar
• Hinds, P. W., and R. A. Weinberg. 1994. Tumor suppressor genes. Curr. Opin. Genet. Dev. 4:135–141.
   PubMed Web of Science ®Google Scholar
• Horowitz, J. M., S.-H. Park, E. Bogenmann, J. C. Cheng, D. W. Yandell, F. J. Kaye, J. D. Minna, T. P. Dryja, and R. A. Weinberg. 1990. Frequent inactivation of the retinoblastoma anti-oncogene is restricted to a subset of human tumor cells. Proc. Nat'l. Acad. Sci. USA. 87:2775–2779.
   PubMed Web of Science ®Google Scholar
• Hurford, R. K., Jr., D. Cobrinik, M.-H. Lee, and N. Dyson. 1997. pRB and p107/p130 are required for the regulated expression of different sets of E2F responsive genes. Genes Dev. 11:1447–1463.
   PubMed Web of Science ®Google Scholar
• Kaye, F. J. 2002. RB and cyclin dependent kinase pathways: defining a distinction between RB and p16 loss in lung cancer. Oncogene 21:6908–6914.
   PubMed Web of Science ®Google Scholar
• Komori, H., M. Enomoto, M. Nakamura, R. Iwanaga, and K. Ohtani. 2005. Distinct E2F-mediated transcriptional program regulates p14(ARF) gene expression. EMBO J. 24:3724–3736.
   PubMed Web of Science ®Google Scholar
• Land, H., L. F. Parada, and R. A. Weinberg. 1983. Tumorigenic conversion of primary embryo fibroblasts requires at least two cooperating oncogenes. Nature 304:596–602.
   PubMed Web of Science ®Google Scholar
• Lee, K. Y., M. H. Ladha, C. McMahon, and M. E. Ewen. 1999. The retinoblastoma protein is linked to the activation of Ras. Mol. Cell. Biol. 19:7724–7732.
   PubMed Web of Science ®Google Scholar
• Leone, G., J. DeGregori, R. Sears, L. Jakoi, and J. R. Nevins. 1997. Myc and Ras collaborate in inducing accumulation of active cyclin E/Cdk2 and E2F. Nature 387:422.
   PubMed Web of Science ®Google Scholar
• Loden, M., F. Perris, N. H. Nielsen, S. O. Emdin, and G. Landberg. 2003. C-erbB2, p27 and G1/S aberrations in human primary breast cancer. Anticancer Res. 23:2053–2061.
   PubMedGoogle Scholar
• Malumbres, M., and A. Pellicer. 1998. RAS pathways to cell cycle control and cell transformation. Front. Biosci. 3:d887–912.
   PubMed Web of Science ®Google Scholar
• Mitchell, P. J., E. Perez-Nadales, D. S. Malcolm, and A. C. Lloyd. 2003. Dissecting the contribution of p16INK4A and the Rb family to the Ras-transformed phenotype. Mol. Cell. Biol. 23:2530–2542.
   PubMedGoogle Scholar
• Mittnacht, S., H. Paterson, M. F. Olson, and C. J. Marshall. 1997. Ras signalling is required for inactivation of the tumour suppressor pRb cell-cycle control protein. Curr. Biol. 7:219–221.
   PubMed Web of Science ®Google Scholar
• Nevins, J. R. 1992. E2F: a link between the Rb tumor suppressor protein and viral oncoproteins. Science 258:424–429.
   PubMed Web of Science ®Google Scholar
• Peeper, D. S., J. H. Dannenberg, S. Douma, H. te Riele, and R. Bernards. 2001. Escape from premature senescence is not sufficient for oncogenic transformation by Ras. Nat. Cell Biol. 3:198–203.
   PubMedGoogle Scholar
• Peeper, D. S., T. M. Upton, M. H. Ladha, E. Neuman, J. Zalvide, R. Bernards, J. A. DeCaprio, and M. E. Ewen. 1997. Ras signalling linked to the cell-cycle machinery by the retinoblastoma protein. Nature 386:177–181.
   PubMed Web of Science ®Google Scholar
• Pierce, A. M., R. Schneider-Broussard, I. B. Gimenez-Conti, J. L. Russell, C. J. Conti, and D. G. Johnson. 1999. E2F1 has both oncogenic and tumor-suppressive properties in a transgenic model. Mol. Cell. Biol. 19:6408–6414.
   PubMed Web of Science ®Google Scholar
• Raychaudhuri, P., S. Bagchi, S. H. Devoto, V. B. Kraus, E. Moran, and J. R. Nevins. 1991. Domains of the adenovirus E1A protein required for oncogenic activity are also required for dissociation of E2F transcription factor complexes. Genes Dev. 5:1200–1211.
   PubMedGoogle Scholar
• Robles, A. I., M. L. Rodriguez-Puebla, A. B. Glick, C. Trempus, L. Hansen, P. Sicinski, R. W. Tennant, R. A. Weinberg, S. H. Yuspa, and C. J. Conti. 1998. Reduced skin tumor development in cyclin D1-deficient mice highlights the oncogenic ras pathway in vivo. Genes Dev. 12:2469–2474.
   PubMed Web of Science ®Google Scholar
• Rodriguez-Puebla, M. L., P. L. Miliani de Marval, M. LaCava, D. S. Moons, H. Kiyokawa, and C. J. Conti. 2002. Cdk4 deficiency inhibits skin tumor development but does not affect normal keratinocyte proliferation. Am. J. Pathol. 161:405–411.
   PubMed Web of Science ®Google Scholar
• Ruiz, S., M. Santos, M. F. Lara, C. Segrelles, C. Ballestin, and J. M. Paramio. 2005. Unexpected roles for pRb in mouse skin carcinogenesis. Cancer Res. 65:9678–9686.
   PubMedGoogle Scholar
• Ruiz, S., M. Santos, C. Segrelles, H. Leis, J. L. Jorcano, A. Berns, J. M. Paramio, and M. Vooijs. 2004. Unique and overlapping functions of pRb and p107 in the control of proliferation and differentiation in epidermis. Development 131:2737–2748.
   PubMedGoogle Scholar
• Ruley, H. E. 1983. Adenovirus early region 1A enables viral and cellular transforming genes to transform primary cells in culture. Nature 304:602–606.
   PubMed Web of Science ®Google Scholar
• Russell, J. L., R. L. Weaks, T. G. Berton, and D. G. Johnson. 3 October 2005, posting date. E2F1 suppresses skin carcinogenesis via the ARF-p53 pathway. Oncogene [Online.] 10.1038/sj.onc.1209120.
   Google Scholar
• Sage, J., A. L. Miller, P. A. Perez-Mancera, J. M. Wysocki, and T. Jacks. 2003. Acute mutation of retinoblastoma gene function is sufficient for cell cycle reentry. Nature 424:223–228.
   PubMed Web of Science ®Google Scholar
• Sage, J., G. J. Mulligan, L. D. Attardi, A. Miller, S. Chen, B. Williams, E. Theodorou, and T. Jacks. 2000. Targeted disruption of the three Rb-related genes leads to loss of G(1) control and immortalization. Genes Dev. 14:3037–3050.
   PubMed Web of Science ®Google Scholar
• Schauer, I. E., S. Siriwardana, T. A. Langan, and R. A. Sclafani. 1994. Cyclin D1 overexpression vs. retinoblastoma inactivation: implications for growth control evasion in non-small cell and small cell lung cancer. Proc. Natl. Acad. Sci. USA 91:7827–7831.
   PubMed Web of Science ®Google Scholar
• Serrano, M., E. Gomez-Lahoz, R. A. DePinho, D. Beach, and D. Bar-Sagi. 1995. Inhibition of Ras-Induced proliferation and cellular transformation by p16Ink4. Science 267:249–252.
   PubMed Web of Science ®Google Scholar
• Serrano, M., H. Lee, L. Chin, C. Cordon-Cardo, D. Beach, and R. A. DePinho. 1996. Role of the INK4a locus in tumor suppression and cell mortality. Cell 85:27–37.
   PubMed Web of Science ®Google Scholar
• Serrano, M., A. W. Lin, M. E. McCurrach, D. Beach, and S. W. Lowe. 1997. Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a. Cell 88:593–602.
   PubMed Web of Science ®Google Scholar
• Sherr, C. J. 2002. D1 in G2. Cell Cycle 1:36–38.
   PubMedGoogle Scholar
• Sotillo, R., J. F. Garcia, S. Ortega, J. Martin, P. Dubus, M. Barbacid, and M. Malumbres. 2001. Invasive melanoma in Cdk4-targeted mice. Proc. Natl. Acad. Sci. USA 98:13312–13317.
   PubMed Web of Science ®Google Scholar
• Stevaux, O., and N. J. Dyson. 2002. A revised picture of the E2F transcriptional network and RB function. Curr. Opin. Cell Biol. 14:684–691.
   PubMed Web of Science ®Google Scholar
• Thomas, D. M., S. A. Carty, D. M. Piscopo, J. S. Lee, W. F. Wang, W. C. Forrester, and P. W. Hinds. 2001. The retinoblastoma protein acts as a transcriptional coactivator required for osteogenic differentiation. Mol. Cell 8:303–316.
   PubMed Web of Science ®Google Scholar
• Thomas, D. M., H. S. Yang, K. Alexander, and P. W. Hinds. 2003. Role of the retinoblastoma protein in differentiation and senescence. Cancer Biol. Ther. 2:124–130.
   PubMed Web of Science ®Google Scholar
• Trimarchi, J. M., and J. A. Lees. 2002. Sibling rivalry in the E2F family. Nat. Rev. Mol. Cell. Biol. 3:11–20.
   PubMed Web of Science ®Google Scholar
• Varley, J. M., J. Armour, J. E. Swallow, A. J. Jeffreys, B. A. Ponder, A. T'Ang, Y. K. Fung, W. J. Brammar, and R. A. Walker. 1989. The retinoblastoma gene is frequently altered leading to loss of expression in primary breast tumours. Oncogene 4:725–729.
   PubMed Web of Science ®Google Scholar
• Walker, G. J., and N. K. Hayward. 2002. Pathways to melanoma development: lessons from the mouse. J. Investig. Dermatol. 119:783–792.
   PubMedGoogle Scholar
• Wang, D., J. L. Russell, and D. G. Johnson. 2000. E2F4 and E2F1 have similar proliferative properties but different apoptotic and oncogenic properties in vivo. Mol. Cell. Biol. 20:3417–3424.
   PubMedGoogle Scholar
• Whyte, P., H. E. Ruley, and E. Harlow. 1988. Two regions of the adenovirus early region 1A proteins are required for transformation. J. Virol. 62:257–265.
   PubMed Web of Science ®Google Scholar
• Williams, J. P., T. Stewart, L. Bihua, R. Mulloy, D. Dimova, and M. Classon. 2006. The retinoblastoma protein is required for Ras-induced oncogenic transformation. Mol. Cell. Biol. 26:1169–1181.
   Google Scholar
• Yamamoto, H., J. W. Soh, T. Monden, M. G. Klein, L. M. Zhang, H. Shirin, N. Arber, N. Tomita, I. Schieren, C. A. Stein, and I. B. Weinstein. 1999. Paradoxical increase in retinoblastoma protein in colorectal carcinomas may protect cells from apoptosis. Clin. Cancer Res. 5:1805–1815.
   PubMed Web of Science ®Google Scholar
• Yu, Q., Y. Geng, and P. Sicinski. 2001. Specific protection against breast cancers by cyclin D1 ablation. Nature 411:1017–1021.
   PubMed Web of Science ®Google Scholar