Cyclin E induction by genotoxic stress leads to apoptosis of hematopoietic cells

Mazumder, Suparna; Gong, Bolin; Almasan, Alexandru

doi:10.1038/sj.onc.1203623

Cited by 57 publications

(53 citation statements)

References 30 publications

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“…As in the case of cyclin B1, examples of cyclin E1 expression outside of the normal cell cycle phase have been reported in pluripotent murine embryonic cells (Stead et al, 2002) and in cells undergoing apoptosis (Mazumder et al, 2000). The cyclin E1 complex was active at 16 h after treatment, which was earlier than cyclin A or cyclin B1 complexes.…”

Section: Discussionmentioning

confidence: 80%

“…Cyclin E protein induction has been identified in IM-9, MOLT-4 and RPMI 8226 cell lines undergoing apoptosis (Mazumder et al, 2000), neuronally derived cells (Padmanabhan et al, 1999), as well as in HT29 cells treated with a novel acronycine derivative (Le´once et al, 2001). B-type cyclins associated with CDK1 have been identified in HL60 cells as they enter apoptosis after treatment with the topoisomerase I inhibitor camptothecin (CPT) (Shimizu et al, 1995) and in epithelial-derived cell lines (Scatena et al, 1998), a HeLa syncytia model (Castedo et al, 2002b) as well as neuronal cells (Shirvan et al, 1998) suggesting that this activity might be required for apoptosis in many different cell types (for review see Castedo et al (2002a)).…”

Section: Introductionmentioning

confidence: 99%

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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: 80%

Section: Introductionmentioning

confidence: 99%

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

et al. 2006

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“…If the level of cyclin E is insufficient, cell cycle arrest at G1/S occurs, while too much cyclin E results in premature entry into S phase, mutations, and genomic instability (Spruck et al, 1999). Irradiation of hematopoietic cancer cells was found to increase cyclin E levels in a time-and dose-dependent manner (Mazumder et al, 2000;Mazumder et al, 2002), and this could influence cell cycle arrest. Importantly, mutations in the F box protein hCDC4 have been implicated in the pathogenesis of various forms of cancer and may be responsible for some cases of elevated cyclin E levels that are frequently associated with human cancers (Koepp et al, 2001;.…”

Section: Cell Cyclementioning

confidence: 99%

The role of the ubiquitin/proteasome system in cellular responses to radiation

et al. 2003

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“…Our group has previously demonstrated that treatment of cells with actinomycin D inhibited a 10-Gy γ-irradiation-induced increase in cell-surface CD20 expression [16]. As treatment of hematopoietic cells with actinomycin D is known to inhibit RNA synthesis, this suggests a transcriptional regulation of CD20 expression rather than a simple alteration in cell-surface morphology or surface presentation of the target antigen [16,17]. …”

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confidence: 98%

Regulation of CD20 expression by radiation-induced changes in intracellular redox status

Gupta

Crosby

Almasan

et al. 2008

Free Radical Biology and Medicine

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Increasing the levels of CD20 expression in cells that harbor low CD20 levels may enhance their responsiveness to CD20-specific antibody therapies. Here, we examined the regulation of CD20 expression after treatment with 0.5-2.0 Gy X-irradiation and hydrogen peroxide (H 2 O 2 ), in the presence or absence of known antioxidants, in the Burkitt lymphoma cell lines Daudi and Raji. Irradiation of cells enhanced cell-surface CD20 expression; the kinetics and extent of this change were cell-type specific and time-dependent. The kinetics of reactive oxygen species generation and changes in mitochondrial membrane potential after irradiation were also correlated with changes in CD20 expression. Raji and Daudi cells treated with H 2 O 2 showed a 2-to 2.5-fold increase in CD20 expression at 12 and 20 h, respectively. Buthionine sulfoximine, which depletes glutathione, also increased surface CD20, whereas antioxidants, such as PEG-catalase, PEG-SOD, vitamin C, and amifostine, decreased CD20 expression induced by radiation or H 2 O 2 . The antioxidant-mediated decrease in CD20 expression induced by radiation or H 2 O 2 suggests a mechanism involving redox regulation. These results demonstrate the critical role of radiationinduced oxidative stress in CD20 expression and may have implications for defining and improving the efficacy of CD20-targeted antibody therapy and radioimmunotherapy. Keywords CD20; Ionizing radiation; Reactive oxygen species; Antioxidants; Mitochondria; Mitochondrial membrane potential; Free radicals The CD20 transmembrane protein is exclusively expressed on B cells. It appears during the pre-B-cell stage, but is absent during the earlier or later stages of B cell differentiation, such as in antibody-secreting plasma cells [1,2]. CD20 has received extensive evaluation as an ideal target for immunotherapy and radioimmunotherapy, in part because of its ubiquitous expression on target cells, stable localization within the cell membrane, and absence from normal stem cells [3]. Rituximab, a chimeric monoclonal anti-CD20 antibody, has been used extensively in the treatment of low-grade B cell lymphomas, such as non-Hodgkin lymphoma (NHL) and other related pathologies. In clinical applications, the efficacy of Rituximab seems to fade after a period of months, leading to Rituximab resistance. The Recent studies have reported that bryostatin-1, interleukin-4, granulocyte-macrophage colony-stimulating factor, tumor necrosis factor-α, and interferon-α are all able to induce CD20 surface expression [8][9][10][11][12][13]. However, the mechanisms regulating the expression of CD20 remain poorly understood, even though these cytokines are well known to cause robust intracellular oxidative bursts [14,15]. Recently, it was shown that the bryostatin-1-induced increase of CD20 was regulated at the transcriptional level. The effect of bryostatin-1 on CD20 expression in NHL-derived cells was apparently mediated through the MAPK/ERK signal transduction pathway and involved protein kinase C [13]. Our group has previous...

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Cyclin E induction by genotoxic stress leads to apoptosis of hematopoietic cells

Cited by 57 publications

References 30 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

The role of the ubiquitin/proteasome system in cellular responses to radiation

Regulation of CD20 expression by radiation-induced changes in intracellular redox status

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