Ras versus cyclin-dependent kinase inhibitors

Current Opinion in Genetics and Development

Volumn 8, Issue 1, 1998, Pages 43-48

  Lloyd, Alison C ^a  

^a UNIVERSITY COLLEGE LONDON   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

CYCLIN DEPENDENT KINASE INHIBITOR; PROTEIN P16; PROTEIN P21; PROTEIN P53; RAS PROTEIN;

CELL CYCLE; CELL PROLIFERATION; CELL TRANSFORMATION; MITOSIS INHIBITION; ONCOGENE RAS; PRIORITY JOURNAL; REVIEW;

EID: 0031936668     PISSN: 0959437X     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0959-437X(98)80060-9     Document Type: Article

References (75)

1. Bos JL. Ras oncogenes in human cancer: a review [published erratum appears in Cancer Res 1990, 50:1352]. Cancer Res. 49:1989;4682-4689.
2. Weinberg RA. Oncogenes, antioncogenes, and the molecular bases of multistep carcinogenesis. Cancer Res. 49:1989;3713-3721.
3. Barbacid M. Ras genes. Annu Rev Biochem. 56:1987;779-827.
4. Ruley HE. Transforming collaborations between ras and nuclear oncogenes. Cancer Cells. 2:1990;258-268.
5. Hunter T. Cooperation between oncogenes. Cell. 64:1991;249-270.
6. Ridley AJ, Paterson HF, Noble M, Land H. Ras-mediated cell cycle arrest is altered by nuclear oncogenes to induce Schwann cell transformation. EMBO J. 7:1988;1635-1645.
7. Lloyd AC, Obermuller F, Staddon S, Barth CF, McMahon M, Land H. Cooperating oncogenes converge to regulate cyclin/cdk complexes. of outstanding interest Genes Dev. 11:1997;663-677 An exploration of the molecular mechanisms involved in the cooperative transformation of primary Schwann cells.
8. Serrano M, Lin AW, McCurrach ME, Beach D, Lowe SW. Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a. of outstanding interest Cell. 88:1997;593-602 Mechanisms underlying the cooperative transformation of primary rodent and human fibroblasts.
9. Wynford-Thomas D. Proliferative lifespan checkpoints: cell-type specificity and influence on tumour biology. Eur J Cancer. 33:1997;716-726.
10. Di Leonardo A, Linke SP, Clarkin K, Wahl GM. DNA damage triggers a prolonged p53-dependent G1 arrest and long-term induction of Cip1 in normal human fibroblasts. Genes Dev. 8:1994;2540-2551.
11. Ko LJ, Prives C. p53: puzzle and paradigm. Genes Dev. 10:1996;1054-1072.
12. Lemoine NR, Staddon S, Bond J, Wyllie FS, Shaw JJ, Wynford TD. Partial transformation of human thyroid epithelial cells by mutant Ha-ras oncogene. Oncogene. 5:1990;1833-1837.
13. -/- cells to Ras transformation.
14. Tanaka N, Ishihara M, Kitagawa M, Harada H, Kimura T, Matsuyama T, Lamphier MS, Aizawa S, Mak TW, Taniguchi T. Cellular commitment to oncogene-induced transformation or apoptosis is dependent on the transcription factor IRF-1. Cell. 77:1994;829-839.
15. Kinzler KW, Vogelstein B. Lessons from hereditary colorectal cancer. Cell. 87:1996;159-170.
16. Caldas C, Hahn SA, Da CL, Redston MS, Schutte M, Seymour AB, Weinstein CL, Hruban RH, Yeo CJ, Kern SE. Frequent somatic mutations and homozygous deletions of the p16 (MTS1) gene in pancreatic adenocarcinoma [published erratum appears in Nat Genet 1994, 8:410]. Nat Genet. 8:1994;27-32.
17. Seymour AB, Hruban RH, Redston M, Caldas C, Powell SM, Kinzler KW, Yeo CJ, Kern SE. Allelotype of pancreatic adenocarcinoma. Cancer Res. 54:1994;2761-2764.
18. Deng C, Zhang P, Harper JW, Elledge SJ, Leder P. Mice lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control. Cell. 82:1995;675-684.
19. Donehower LA, Harvey M, Slagle BL, McArthur MJ, Montgomery CJ, Butel JS, Bradley A. Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours. Nature. 356:1992;215-221.
20. Brugarolas J, Chandrasekaran C, Gordon JI, Beach D, Jacks T, Hannon GJ. Radiation-induced cell cycle arrest compromised by p21 deficiency. Nature. 377:1995;552-557.
21. -/- or wild-type mice, become highly transformed and tumourigenic when infected with Ras-expressing retroviruses.
22. Cip1 induction, by high levels of Raf activity, is responsible for the growth arrest.
23. Cip1. of special interest Mol Cell Biol. 17:1997;5598-5611 See annotation [22].
24. Cip1 bypass normal senescence.
25. 1 arrests in response to DNA damage into a cell line that responds by undergoing apoptosis by inactivating p21 by homologous recombination.
26. Hermeking H, Funk JO, Reichert M, Ellwart JW, Eick D. Abrogation of p53-induced cell cycle arrest by c-Myc: evidence for an inhibitor of p21WAF1/CIP1/SDl1. Oncogene. 11:1995;1409-1415.
27. INK4. Science. 267:1995;249-252.
28. INK4A-induced cell-cycle arrest.
29. Cip1 by DNA damage requires both p53 and IRF1.
30. Vousden KH. Regulation of the cell cycle by viral oncoproteins. Semin Cancer Biol. 6:1995;109-116.
31. Lill NL, Grossman SR, Ginsberg D, DeCaprio J, Livingstone DM. Binding and modulation of p53 by p300/CBP coactivators. of outstanding interest Nature. 387:1997;823-827 One of three papers showing that p300/CBP act as transcriptional coactivators of p53. See also [32,33].
32. Gu W, Shi X-L, Roeder RG. Synergistic activation of transcription by CBP and p53. of outstanding interest Nature. 387:1997;819-823 See annotation [31].
33. Avantaggiati ML, Ogryzko O, Gardner K, Giordano A, Levine AS, Kelly K. Recruitment of p300/CBP in p53-dependent signal pathways. of outstanding interest Cell. 89:1997;1175-1184 See annotation [31].
34. Cip1.
35. Cip1, which, as a consequence, becomes active.
36. Lovec H, Sewing A, Lucibello FC, Muller R, Moroy T. Oncogenic activity of cyclin D1 revealed through cooperation with Ha-ras; link between cell cycle control and malignant transformation. Oncogene. 9:1994;323-326.
37. Galaktionov K, Lee AK, Eckstein J, Draetta G, Meckler J, Loda M, Beach D. CDC25 phosphatases as potential human oncogenes. Science. 269:1995;1575-1577.
38. INK4b genes. Oncogene. 11:1995;635-645.
39. Perez-Roger I, Solomon DLC, Sewing A, Land H. Myc activation of cyclin/Cdk2 kinase involves induction of cyclin E gene transcription and inhibition of p27 binding to newly formed complexes. Oncogene. 14:1997;2373-2381.
40. Franza BJ, Maruyama K, Garrels JI, Ruley HE. In vitro establishment is not a sufficient prerequisite for transformation by activated ras oncogenes. Cell. 44:1986;409-418.
41. Bottazzi ME, Assoian RK. The extracellular matrix and mitogenic growth factors control G1 phase cyclins and cyclin-dependent kinase inhibitors. Trends Cell Biol. 7:1997;348-352.
42. Miyamoto S, Teramoto H, Gutkind JS, Yamada KM. Integrins can collaborate with growth factors for phosphorylation of receptor tyrosine kinases and MAP kinase activation: roles of integrin aggregation and occupancy of receptors. J Cell Biol. 135:1996;1633-1642.
43. Zhu X, Assoian RK. Integrin-dependent activation of MAP kinase: a link to shape-dependent cell proliferation [published erratum appears in Mol Biol Cell 1996, 7:1001]. Mol Biol Cell. 6:1995;273-282.
44. Mansour SJ, Matten WT, Hermann AS, Candia JM, Rong S, Fukasawa K, Vande WG, Ahn NG. Transformation of mammalian cells by constitutively active MAP kinase kinase. Science. 265:1994;966-970.
45. Cowley S, Paterson H, Kemp P, Marshall CJ. Activation of MAP kinase kinase is necessary and sufficient for PC12 differentiation and for transformation of NIH 3T3 cells. Cell. 77:1994;841-852.
46. Inoue H, Yamashita A, Hakura A. Adhesion-dependency of serum-induced p42/p44 MAP kinase activation is released by retroviral oncogenes. of special interest Virology. 225:1996;223-226 Ras-transformed cells have constitutively high MAP kinase activity in the absence of mitogens or anchorage.
47. Lavoie JN, L'Allemain G, Brunet A, Muller R, Pouyssegur J. Cyclin D1 expression is regulated positively by the p42/p44MAPK and negatively by the p38/HOGMAPK pathway. of special interest J Biol Chem. 271:1996;20608-20616 A correlation between persistent activation of the MAP kinase pathway and cyclin D1 induction and proliferation.
48. Kang JS, Krauss RS. Ras induces anchorage-independent growth by subverting multiple adhesion-regulated cell cycle events. of special interest Mol Cell Biol. 16:1996;3370-3380 A dissociation of the requirement for cyclin A induction from cyclin E- and D-dependent kinase activity for anchorage-independent growth.
49. Winston JT, Coats SR, Wang YZ, Pledger WJ. Regulation of the cell cycle machinery by oncogenic ras. of special interest Oncogene. 12:1996;127-130 Factors in plasma and Ras synergise to suppress p27 and induce Balb 3T3 cells into the cycle.
50. Filmus J, Robles AI, Shi W, Wong MJ, Colombo LL, Conti CJ. Induction of cyclin D1 overexpression by activated ras. Oncogene. 9:1994;3627-3633.
51. Albanese C, Johnson J, Watanabe G, Eklund N, Vu D, Arnold A, Pestell RG. Transforming p21ras mutants and c-Ets-2 activate the cyclin D1 promoter through distinguishable regions. J Biol Chem. 270:1995;23589-23597.
52. Arber N, Sutter T, Miyake M, Kahn SM, Venkatraj VS, Sobrino A, Warburton D, Holt PR, Weinstein IB. Increased expression of cyclin D1 and the Rb tumor suppressor gene in c-K-ras transformed rat enterocytes. Oncogene. 12:1996;1903-1908.
53. Liu JJ, Chao JR, Jiang MC, Ng SY, Yen JJ, Yang YH. Ras transformation results in an elevated level of cyclin D1 and acceleration of G1 progression in NIH 3T3 cells. Mol Cell Biol. 15:1995;3654-3663.
54. Zhu X, Ohtsubo M, Bohmer RM, Roberts JM, Assoian RK. Adhesion-dependent cell cycle progression linked to the expression of cyclin D1, activation of cyclin E-cdk2, and phosphorylation of the retinoblastoma protein. of special interest J Cell Biol. 133:1996;391-403 A characterisation of the cell-cycle checkpoints associated with loss of anchorage.
55. Resnitzky D. Ectopic expression of cyclin D1 but not cyclin E induces anchorage-independent cell cycle progression. Mol Cell Biol. 17:1997;5640-5647.
56. Downward J. Cell cycle: routine role for Ras. Curr Biol. 7:1997;258-260.
57. Kip1.
58. Leone G, DeGregori J, Sears R, Jakoi L, Nevins JR. Myc and Ras collaborate in inducing accumulation of active cyclin E/Cdk2 and E2F. of outstanding interest Nature. 387:1997;422-426 Ras and Myc synergise to induce DNA synthesis in REF52 cells by inducing cyclin E-dependent kinase as a result of suppressing p27. Surprisingly, these cells cycle in the absence of cyclin D-associated kinase activity and with Rb in the hypophosphorylated state.
59. Mittnacht S, Paterson H, Olson MF, Marshall CJ. Ras signalling is required for inactivation of the tumour suppressor pRb cell-cycle control protein. of special interest Curr Biol. 7:1997;219-221 See annotation [60].
60. 1 phase transition.
61. Polyak K, Kato JY, Solomon MJ, Sherr CJ, Massague J, Roberts JM, Koff A. p27Kip1, a cyclin-Cdk inhibitor, links transforming growth factor-beta and contact inhibition to cell cycle arrest. Genes Dev. 8:1994;9-22.
62. Coats S, Flanagan WM, Nourse J, Roberts JM. Requirement of p27Kip1 for restriction point control of the fibroblast cell cycle. Science. 272:1996;877-880.
63. Kip1, resulting in an inhibition of cyclin E-dependent kinase activity.
64. Kato A, Takahashi H, Takahashi Y, Matsushime H. Inactivation of the cyclin D-dependent kinase in the rat fibroblast cell line, 3Y1, induced by contact inhibition. J Biol Chem. 272:1997;8065-8070.
65. 0 state) in fibroblasts. J Biol Chem. 271:1996;18337-18341.
66. Kip1 which is then unable to bind and inhibit CDK activity.
67. 1.
68. Guadagno TM, Ohtsubo M, Roberts JM, Assoian RK. A link between cyclin A expression and adhesion-dependent cell cycle progression [published erratum appears in Science 1994, 263:455]. Science. 262:1993;1572-1575.
69. Pumiglia KM, Decker SJ. Cell cycle arrest mediated by the MEK/mitogen-activated protein kinase pathway. Proc Natl Acad Sci USA. 94:1997;448-452.
70. Jakus J, Yeudall WA. Growth inhibitory concentrations of EGF induce p21 (WAF1/Cip1) and alter cell cycle control in squamous carcinoma cells. Oncogene. 12:1996;2369-2376.
71. Joneson T, White MA, Wigler MH, Bar SD. Stimulation of membrane ruffling and MAP kinase activation by distinct effectors of RAS. of special interest Science. 271:1996;810-812 Mutants of Ras that interact only with specific effectors were used to demonstrate that the MAP kinase pathway and the Pl3 kinase pathway synergise to induce DNA synthesis.
72. Rodriguez VP, Warne PH, Khwaja A, Marte BM, Pappin D, Das P, Waterfield MD, Ridley A, Downward J. Role of phosphoinositide 3-OH kinase in cell transformation and control of the actin cytoskeleton by Ras. of outstanding interest Cell. 89:1997;457-467 A demonstration of the importance of the Pl3 kinase signalling pathway downstream from Ras for Ras-induced focus formation and anchorage-independent growth.
73. Frisch SM, Ruoslahti E. Integrins and anoikis. Curr Opin Cell Biol. 9:1997;701-706.
74. Khwaja A, Rodriguez VP, Wennstrom S, Warne PH, Downward J. Matrix adhesion and Ras transformation both activate a phosphoinositide 3-OH kinase and protein kinase B/Akt cellular survival pathway. of outstanding interest EMBO J. 16:1997;2783-2793 Ras protects epithelial cells from anoikis through its Pl3 kinase signalling pathways.
75. ARF. Cell. 91:1997;649-659.