Isolation of a human cyclin cDNA: Evidence for cyclin mRNA and protein regulation in the cell cycle and for interaction with p34cdc2

Pines, Jonathon; Hunter, Tony

doi:10.1016/0092-8674(89)90936-7

Cited by 883 publications

(639 citation statements)

References 46 publications

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“…We chose to use the topoisomerase I inhibitor, CPT, at 1 mM by which 93% of HT 29 cells are in apoptosis in 72 h. At concentrations of around 100 nM, CPT induces a G2/M-phase block in the cell cycle by activating a DNA damage checkpoint ( (Tanizawa et al, 1994), data not shown). Whereas these cells also enter apoptosis, it is more difficult to characterize a putative apoptosis-specific activity of cyclin B1/CDK1 complex in G2/M-phase cells because cyclin B1 protein levels are already elevated as compared to G1 cells where cyclin B1 levels are very low (Pines and Hunter, 1989). Therefore, we used higher concentrations of CPT, as have been previously reported in the literature (Smits et al, 2000;Furuta et al, 2003), at which cells were blocked in all major phases of the cell cycle.…”

Section: Discussionmentioning

confidence: 99%

Analysis of cyclin B1 and CDK activity during apoptosis induced by camptothecin treatment

et al. 2006

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We have studied the role of cyclins and cyclin-dependent kinase (CDK) activity in apoptosis induced by camptothecin (CPT). In this model, 22% of the cells stain for annexin-V at 24 h and then proceed to be 93% positive by 72 h. This time window permits the analysis of cyclins in cells that are committed to apoptosis but not yet dead. We provide evidence that cyclin protein levels and then associated kinase levels increase after CPT treatment. Strikingly, cyclin B1 and cyclin E1 proteins are present at the same time in CPT treated HT29 cells. Although cyclin B1 and E1 CDK complexes are activated in CPT treated cells, only the cyclin B1 complex is required for apoptosis since reduction of cyclin B1 by RNAi or roscovitine treatment reduces the number of annexin-V-stained cells. We have detected poorly organized chromosomes and phosphorylated histone H3 epitopes at the time of maximum cyclin B1/CDK kinase activity in CPT-treated cells, which suggests that these cells enter a mitotic catastrophe. Understanding which CDKs are required for apoptosis may allow us to better adapt CDK inhibitors for use as anti-cancer compounds.

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Section: Discussionmentioning

confidence: 99%

Analysis of cyclin B1 and CDK activity during apoptosis induced by camptothecin treatment

et al. 2006

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“…Cyclin B1 is downregulated and contributes to the enrichment of the cell cycle GO category. Cyclin B1 is known to be expressed predominantly in the G2/M phase of cell division (Pines and Hunter, 1989). Finally the hub UBE2 complex contains both downregulated genes and predicted mir-21 targets according to the PITA algorithm (John et al, 2004;Kertesz et al, 2007).…”

Section: Regulation Of Mir-21 By Ras and Its Role In Cancer D Frezzetmentioning

confidence: 99%

Upregulation of miR-21 by Ras in vivo and its role in tumor growth

et al. 2010

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miR-21 is a microRNA (miRNA) frequently overexpressed in human cancers. Here we show that miR-21 is upregulated both in vitro and in vivo by oncogenic Ras, thus linking this miRNA to one of the most frequently activated oncogenes in human cancers. Ras regulation of miR-21 occurs with a delayed kinetic and requires at least two Ras downstream pathways. A screen of human thyroid cancers and non-small-cell lung cancers for the expression of miR-21 reveals that it is overexpressed mainly in anaplastic thyroid carcinomas, the most aggressive form of thyroid cancer, whereas in lung its overexpression appears to be inversely correlated with tumor progression. We also show that a LNA directed against miR-21 slows down tumor growth in mice. Consistently, a search for mRNAs downregulated by miR-21 shows an enrichment for mRNAs encoding cell cycle checkpoints regulators, suggesting an important role for miR-21 in oncogenic Ras-induced cell proliferation.

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“…Once in the G 2 phase of the cycle, cyclin A binds and forms an active kinase complex with CDK1 that help cells to transit into mitosis. Progression through the M phase requires the activity of another phase-specific complex, cyclin B-CDK1 (Pines and Hunter, 1989). A recent report shows CDK1 phosphorylates peroxiredoxin I inhibiting its oxidase activity.…”

Section: Intracellular Redox State and Cell Cycle Proteinsmentioning

confidence: 99%

A redox cycle within the cell cycle: ring in the old with the new

2006

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In recent years, the intracellular oxidation-reduction (redox) state has gained increasing attention as a critical mediator of cell signaling, gene expression changes and proliferation. This review discusses the evidence for a redox cycle (i.e., fluctuation in the cellular redox state) regulating the cell cycle. The presence of redox-sensitive motifs (cysteine residues, metal co-factors in kinases and phosphatases) in several cell cycle regulatory proteins indicate periodic oscillations in intracellular redox state could play a central role in regulating progression from G 0 /G 1 to S to G 2 and M cell cycle phases. Fluctuations in the intracellular redox state during cell cycle progression could represent a fundamental mechanism linking oxidative metabolic processes to cell cycle regulatory processes. Proliferative disorders are central to a variety of human pathophysiological conditions thought to involve oxidative stress. Therefore, a more complete understanding of redox control of the cell cycle could provide a biochemical rationale for manipulating aberrant cell proliferation.

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Isolation of a human cyclin cDNA: Evidence for cyclin mRNA and protein regulation in the cell cycle and for interaction with p34cdc2

Cited by 883 publications

References 46 publications

Analysis of cyclin B1 and CDK activity during apoptosis induced by camptothecin treatment

Analysis of cyclin B1 and CDK activity during apoptosis induced by camptothecin treatment

Upregulation of miR-21 by Ras in vivo and its role in tumor growth

A redox cycle within the cell cycle: ring in the old with the new

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