Ras and Rho regulation of the cell cycle and oncogenesis

Cancer Letters

Volumn 171, Issue 1, 2001, Pages 1-10

  Pruitt, Kevin ^a   Der, Channing J ^a  

^a UNIVERSITY OF NORTH CAROLINA   (United States)

Author keywords

Cyclin D1; p21CIP1; p27KIP1; Rac; Raf; Rho

Indexed keywords

CYCLIN D1; CYCLIN DEPENDENT KINASE INHIBITOR; PROTEIN P21; PROTEIN P27; RAS PROTEIN; RHO GUANINE NUCLEOTIDE BINDING PROTEIN;

CARCINOGENESIS; CELL CYCLE; NONHUMAN; ONCOGENE RAS; PRIORITY JOURNAL; REGULATORY MECHANISM; SHORT SURVEY; SIGNAL TRANSDUCTION;

EID: 0035964458     PISSN: 03043835     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0304-3835(01)00528-6     Document Type: Review

References (85)

1. Increasing complexity of Ras signaling
2. Understanding Ras: 'It ain't over 'til it's over'
3. Ras and Rho GTPases: A family reunion
4. C.D.K. inhibitors: Positive and negative regulators of G1-phase progression
5. The Rb/E2F pathway: Expanding roles and emerging paradigms
6. Cell cycle: Routine role for Ras
7. Cell cycle targets of Ras/Raf signalling
8. How do small GTPase signal transduction pathways regulate cell cycle entry?
9. Proteins regulating Ras and its relatives
10. Ras genes
11. Oncogenic activation of Ras proteins
12. Ras effectors
13. Ras signalling and apoptosis
14. Ras caught in another affair: The exchange factors for Ral
15. Ras uses the novel tumor suppressor RASSF1 as an effector to mediate apoptosis
16. Phospholipase C(epsilon): A novel Ras effector
17. Requirement for ras proto-oncogene function during serum-stimulated growth of NIH 3T3 cells
18. Inhibition of NIH 3T3 cell proliferation by a mutant ras protein with preferential affinity for GDP
19. Effect of a dominant inhibitory Ha-ras mutation o mitogenic signal transduction in NIH 3T3 cells
20. Cellular ras activity is required for passage through multiple points of the G0/G1 phase in the BALB/c 3T3 cells
21. Transformation of NIH/3T3 cells by microinjection of Ha-ras p21 protein
22. Accumulation of p21ras. GTP in response to stimulation with epidermal growth factor and oncogene products with tyrosine kinase activity
23. Cell cycle-dependent activation of Ras
24. Multiple ras effector pathways contribute to G(1) cell cycle progression
25. Ras signalling linked to the cell-cycle machinery by the retinoblastoma protein
26. Ras signalling is required for inactivation of the tumour suppressor pRb cell-cycle control protein
27. Transformation-restoring factor: A low molecular weight secreted factor required for anchorage-independent growth of oncogene-resistant mutant cell lines
28. Ras induces anchorage-independent growth by subverting multiple adhesion-regulated cell cycle events
29. Ras inactivation of the retinoblastoma pathway by distinct mechanisms in NIH 3T3 fibroblast and RIE-1 epithelial cells
30. Rho family proteins and Ras transformation: The RHOad less travelled gets congested
31. Rho signals to cell growth and apoptosis
32. Ras-dependent cell cycle commitment during G2 phase
33. Colony-stimulating factor 1 regulates novel cyclins during the G1 phase of the cell cycle
34. Ras links growth factor signaling to the cell cycle machinery via regulation of cyclin D1 and the Cdk inhibitor p27KIP1
35. Identification and characterization of potential effector molecules of the Ras-related GTPase Rap2
36. Regulation of the cell cycle machinery by oncogenic ras
37. Oncogenic Ras-mediated cell growth arrest and apoptosis is associated with increased ubiquitin-dependent cyclin D1 degradation
38. Ras transformation results in an elevated level of cyclin D1 and acceleration of G1 progression in NIH 3T3 cells
39. Increased expression of cyclin D1 and the Rb tumor suppressor gene in c- K-ras transformed rat enterocytes
40. Ras signals to the cell cycle machinery via multiple pathways to induce anchorage-independent growth
41. Induction of cyclin D1 overexpression by activated ras
42. Cyclin D1 expression is regulated positively by the p42/p44MAPK and negatively by the p38/HOGMAPK pathway
43. Induction of cell proliferation in quiescent NIH 3T3 cells by oncogenic c-Raf-1
44. Inactivation of Rho signaling pathway promotes CNS axon regeneration
45. Regulation of exit from quiescence by p27 and cyclin D1-CDK4
46. Transforming p21ras mutants and c-Ets-2 activate the cyclin D1 promoter through distinguishable regions
47. Beta-catenin regulates expression of cyclin D1 in colon carcinoma cells
48. Ral GTPases contribute to regulation of cyclin D1 through activation of NF-kappaB
49. Glycogen synthase kinase-3beta regulates cyclin D1 proteolysis and subcellular localization
50. Cyclin D expression is controlled post-transcriptionally via a phosphatidylinositol 3-kinase/Akt-dependent pathway
51. Cooperating oncogenes converge to regulate cyclin/cdk complexes
52. Cell cycle arrest mediated by the MEK/mitogen-activated protein kinase pathway
53. High-intensity Raf signal causes cell cycle arrest mediated by p21Cip1
54. Raf-induced proliferation or cell cycle arrest is determined by the level of Raf activity with arrest mediated by p21Cip1
55. Signals from Ras and Rho GTPases interact to regulate expression of p21Waf1/Cip1
56. The absence of p21Cip1/WAF1 alters keratinocyte growth and differentiation and promotes ras-tumor progression
57. Cross-talk between Ras and Rho signalling pathways in transformation favours proliferation and increased motility
58. p21-containing cyclin kinases exist in both active and inactive states
59. Formation of p27-CDK complexes during the human mitotic cell cycle
60. Differential interaction of the cyclin-dependent kinase (Cdk) inhibitor p27Kip1 with cyclin A-Cdk2 and cyclin D2-Cdk4
61. New functional activities for the p21 family of CDK inhibitors
62. Regulation of the cdk inhibitor p27 and its deregulation in cancer
63. Ras activity late in G1 phase required for p27kip1 downregulation, passage through the restriction point, and entry into S phase in growth factor-stimulated NIH 3T3 fibroblasts
64. Kip1 accumulation during the cell cycle
65. Role of the ubiquitin-proteasome pathway in regulating abundance of the cyclin-dependent kinase inhibitor p27
66. Kip1 degradation and induces S phase in quiescent cells
67. An analysis of Mek1 signaling in cell proliferation and transformation
68. Regulation of the cyclin-dependent kinase inhibitor p27 by degradation and phosphorylation
69. Kip1 regulated by mitogen-activated protein kinase kinase (MEK1)
70. Myc and Ras collaborate in inducing accumulation of active cyclin E/Cdk2 and E2F
71. Rho GTPases and signaling networks
72. Rho GTPases and their effector proteins
73. ADP-ribosylation of the rhoA gene product by botulinum C3 exoenzyme causes Swiss 3T3 cells to accumulate in the G1 phase of the cell cycle
74. An essential role for Rho, Rac and Cdc42 GTPases in cell cycle progression through G1
75. Regulation of c-myc expression by Ras/Raf signalling
76. The geranylgeranyltransferase-I inhibitor GGTI-298 arrests human tumor cells in G0/G1 and induces p21WAF1/CIP1/SDI1 in a p53-independent manner
77. Rac regulation of transformation, gene expression, and actin organization by multiple, PAK-independent pathways
78. Transforming potential of Dbl family proteins correlates with transcription from the cyclin D1 promoter but not with activation of Jun NH2-terminal kinase, p38/Mpk2, serum response factor or c-Jun
79. Integration of Rac-dependent regulation of cyclin D1 transcription through a nuclear factor-kappaB-dependent pathway
80. Rac and Cdc42 are potent stimulators of E2F-dependent transcription capable of promoting retinoblastoma susceptibility gene product hyperphosphorylation
81. Signals from Ras and Rho GTPases interact to regulate expression of p21Waf1/Cip1
82. Ras-stimulated extracellular signal-related kinase 1 and RhoA activities coordinate platelet-derived growth factor-induced G1 progression through the independent regulation of cyclin D1 and p27
83. RhoA stimulates p27(Kip) degradation through its regulation of cyclin E/CDK2 activity
84. Geranylgeranylated Rho small GTPase(s) are essential for the degradation of p27Kip1 and facilitate the progression from G1 to S phase in growth-stimulated rat FRTL-5 cells
85. Rho signals to cell growth and apoptosis