Loss of p27(Kip1) from cyclin E/cyclin-dependent kinase (CDK) 2 but not from cyclin D1/CDK4 complexes in cells transformed by polyamine biosynthetic enzymes

Cancer Research

Volumn 60, Issue 18, 2000, Pages 5244-5253

  Ravanko, K ^a   Jarvinen, K ^a   Paasinen Sohns, A ^a   Holtta, E ^a  

^a UNIVERSITY OF HELSINKI   (Finland)

Author keywords

[No Author keywords available]

Indexed keywords

ADENOSYLMETHIONINE DECARBOXYLASE; CYCLIN D1; CYCLIN DEPENDENT KINASE 2; CYCLIN DEPENDENT KINASE 4; CYCLIN E; ORNITHINE DECARBOXYLASE; POLYAMINE; PROTEIN P27; RETINOBLASTOMA PROTEIN; CDK2 PROTEIN, HUMAN; CDK2 PROTEIN, MOUSE; CDK2 PROTEIN, RAT; CDK4 PROTEIN, HUMAN; CDK4 PROTEIN, MOUSE; CDK4 PROTEIN, RAT; CDKN1B PROTEIN, MOUSE; CDKN1B PROTEIN, RAT; CELL CYCLE PROTEIN; COMPLEMENTARY DNA; CYCLIN DEPENDENT KINASE; CYCLIN DEPENDENT KINASE INHIBITOR 1B; MICROTUBULE ASSOCIATED PROTEIN; ONCOPROTEIN; PROTEIN SERINE THREONINE KINASE; TUMOR SUPPRESSOR PROTEIN;

ANIMAL CELL; ARTICLE; CARCINOGENESIS; CELL CYCLE; CELL PROLIFERATION; CELL STRAIN 3T3; CELL TRANSFORMATION; COMPLEX FORMATION; DOWN REGULATION; ENZYME ANALYSIS; FIBROBLAST; MOUSE; NONHUMAN; POLYAMINE SYNTHESIS; PRIORITY JOURNAL; ANIMAL; BIOSYNTHESIS; CELL DIVISION; CYTOLOGY; ENZYMOLOGY; GENE EXPRESSION PROFILING; GENETIC TRANSFECTION; GENETICS; HUMAN; METABOLISM; NORTHERN BLOTTING; NUDE MOUSE; PHOSPHORYLATION; PHYSIOLOGY; PLASMID; RAT;

3T3 CELLS; ADENOSYLMETHIONINE DECARBOXYLASE; ANIMALS; BLOTTING, NORTHERN; CDC2-CDC28 KINASES; CELL CYCLE; CELL CYCLE PROTEINS; CELL DIVISION; CELL TRANSFORMATION, NEOPLASTIC; CYCLIN D1; CYCLIN E; CYCLIN-DEPENDENT KINASE 2; CYCLIN-DEPENDENT KINASE 4; CYCLIN-DEPENDENT KINASE INHIBITOR P27; CYCLIN-DEPENDENT KINASES; DNA, COMPLEMENTARY; GENE EXPRESSION PROFILING; HUMANS; MICE; MICE, NUDE; MICROTUBULE-ASSOCIATED PROTEINS; ORNITHINE DECARBOXYLASE; PHOSPHORYLATION; PLASMIDS; PROTEIN-SERINE-THREONINE KINASES; PROTO-ONCOGENE PROTEINS; RATS; RETINOBLASTOMA PROTEIN; TRANSFECTION; TUMOR SUPPRESSOR PROTEINS;

EID: 0034664256     PISSN: 00085472     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (88)

1. Cancer cell cycles
2. 1 phase progression: Cycling on cue
3. D-type cyclin-dependent kinase activity in mammalian cells
4. 1 kinase activity for cdk6, a novel cyclin D partner
5. Principles of CDK regulation
6. 1 cyclin-dependent kinases
7. p21 Is a universal inhibitor of cyclin kinases
8. 1 cyclin-dependent kinases
9. Cloning of p27(Kip1), a cyclin-dependent kinase inhibitor and a potential mediator of extracellular antimitogenic signals
10. 1 cyclin-Cdk protein kinase activity, is related to p21
11. 1-S phase protein kinase
12. 1 phase of the human cell cycle
13. Cyclin E-CDK2 is a regulator of p27(Kip1)
14. Expression of NPAT, a novel substrate of cyclin E-CDK2, promotes S-phase entry
15. Functional inactivation of the retinoblastoma protein requires sequential mortification by at least two distinct cyclin-cdk complexes
16. Rescue of cyclin D1 deficiency by knockin cyclin E
17. 1
18. Cyclins and cancer. II. Cyclin D and CDK inhibitors come of age
19. Cyclin E in human cancers
20. Subunit rearrangement of the cyclin-dependent kinase is associated with cellular transformation
21. Alteration of cell cycle kinase complexes in human papillomavirus E6- and E7-expressing fibroblasts precedes neoplastic transformation
22. Mutations in the p53 tumor suppressor gene: Clues to cancer etiology and molecular pathogenesis
23. Frequent inactivation of the retinoblastoma anti-oncogene is restricted to a subset of human tumor cells
24. The INK4a/ARF tumor suppressor: One gene two products two pathways
25. The p16(INK4a)/CDKN2A tumor suppressor and its relatives
26. Tumor surveillance via the ARF-p53 pathway
27. Recent advances in the biochemistry of polyamines in eucaryotes
28. Molecular genetics of polyamine synthesis in eukaryotic cells
29. Polyamines are essential for cell transformation by pp60(v-src): Delineation of molecular events relevant for the trans-formed phenotype
30. Activation of chimeric EGF-R/neu tyrosine kinase induces the fos/jun transcription factor complex, glucose transporter and ornithine decarboxylase
31. The mechanisms of ornithine decarboxylase deregulation in c-Ha-ras oncogene-transformed NIH 3T3 cells
32. Ornithine decarboxylase activity is critical for cell transformation
33. Human ornithine decarboxylase-overproducing NIH3T3 cells induce rapidly growing, highly vascularized tumors in nude mice
34. Advanced mammalian gene transfer: High titre retroviral vectors with multiple drug selection markers and a complementary helper-free packaging cell line
35. Increased expression of cyclin D2 during multiple states of growth arrest in primary and established cells
36. 1/S transition and high abundance in quiescent tissues suggest a dual role in proliferation and differentiation
37. Ras links growth factor signaling to the cell cycle machinery via regulation of cyclin D1 and the Cdk inhibitor p27(KIP1)
38. Cdk2-dependent phosphorylation of p27 facilitates its Myc-induced release from cyclin E/cdk2 complexes
39. Expression of the v-Src oncoprotein in fibroblasts disrupts normal regulation of the CDK inhibitor p27 and inhibits quiescence
40. The ornithine decarboxylase is a transcriptional target of c-Myc
41. Polyamine depletion arrests cell cycle and induces inhibitors p21(Waf1/Cip1), p27(Kip1) and p53 in IEC-6 cells
42. Down-regulation of p27(Kip1) by two mechanisms, ubiquitin-mediated degradation and proteolytic processing
43. High-intensity Raf signal causes cell cycle arrest mediated by p21(Cip1)
44. Raf-induced proliferation or cell cycle arrest is determined by the level of Raf activity with-arrest mediated by p21(Cip1)
45. c-Myc regulates cyclin D-Cdk4 and -Cdk6 activity but affects cell cycle progression at multiple independent points
46. The p21(Cip1) and p27(Kip1) CDK 'inhibitors' are essential activators of cyclin D-dependent kinases in murine fibroblasts
47. New functional activities for the p21 family of CDK inhibitors
48. Involvement of polyamines in retinoblastoma protein phosphorylation
49. 1 arrest in human melanoma cells
50. Creation of human tumour cells with defined genetic elements
51. Development of difluoromethylornithine (DFMO) as a chemoprevention agent
52. Role of ornithine decarboxylase in epidermal tumorigenesis
53. Ornithine decarboxylase overexpression is a sufficient condition for tumor promotion in mouse skin
54. Cell transformation by ornithine decarboxylase is associated with phosphorylation of the transactivation domain of c-Jun
55. 1 progression in NIH 3T3 cells
56. Frequent overexpression of the cyclin D1 oncogene in invasive lobular carcinoma of the breast
57. Reduced skin tumor development in cyclin D1-deficient mice highlighs the oncogenic ras pathway in vivo
58. Mammary hyperplasia and carcinoma in MMTV-cyclin D1 transgenic mice
59. The cyclin D1 gene is a target of the β-catenin/LEF-1 pathway
60. Antisense to cyclin D1 inhibits the growth and tumorigenicity of human colon cancer cells
61. Gene expression and cell cycle arrest mediated by transcription factor DMP1 is antagonized by D-type cyclins through a cyclin-dependent-kinase-independent mechanism
62. CDK-independent activation of estrogen receptor by cyclin D 1
63. Cyclin D1 stimulation of estrogen receptor transcriptional activity independent of cdk4
64. Ras signalling linked to the cell-cycle machinery by the retinoblastoma protein
65. Myc and Ras collaborate in inducing accumulation of active cyclin E/Cdk2 and E2F
66. Loss of cyclin-dependent kinase inhibitor p27(Kip1) is a novel prognostic factor in localized human prostate adenocarcinomas
67. Association of p27(Kip1) levels with recurrence and survival in patients with stage C prostate carcinoma
68. Decreased levels of the cell-cycle inhibitor p27(Kip1) protein: Prognostic implications in primary breast cancer
69. Prognostic role of the cyclin-dependent kinase inhibitor p27 in non-small cell lung cancer
70. Increased proteasome-dependent degradation of the cyclindependent kinase inhibitor p27 in aggressive colorectal carcinomas
71. p27 Expression and gastric carcinoma
72. Reduced levels of the cell-cycle inhibitor p27(Kip1) in epithelial dysplasia and carcinoma of the oral cavity
73. p27(Kip1): A multifunctional cyclin-dependent kinase inhibitor with prognostic significance in human cancers
74. The prognostic significance of altered cyclin-dependent kinase inhibitors in human cancer
75. The murine gene p27(Kip1) is haplo-insufficient for tumour suppression
76. A syndrome of multiorgan hyperplasia with features of gigantism, tumorigenesis, and female sterility in p27(Kip1)-deficient mice
77. Enhanced growth of mice lacking the cyclin-dependent kinase inhibitor function of p27(Kip1)
78. Mice lacking p27(Kip1) display increased body size, multiple organ hyperplasia, retinal dysplasia, and pituitary tumors
79. Role of the ubiquitin-proteasome pathway in regulating abundance of the cyclin-dependent kinase inhibitor p27
80. 1 growth arrest
81. Ubiquitination of p27 is regulated by Cdk-dependent phosphorylation and trimeric complex formation
82. Phosphorylation-dependent degradation of the cyclin-dependent kinase inhibitor p27(Kip1)
83. Mechanism of Cdk2/cyclin E inhibition by p27 and p27 phosphorylation
84. Direct induction of cyclin D2 by Myc contributes to cell cycle progression and sequestration of p27
85. Cyclins D1 and D2 mediate Myc-induced proliferation via sequestration of p27(Kip1) and p21(Cip1)
86. The cyclin-dependent kinase inhibitor p27(Kip1) induces N-terminal proteolytic cleavage of cyclin A
87. Effect of elevated levels of ornithine decarboxylase on cell cycle progression in skin