Control of cell cycle progression in human mesothelioma cells treated with gamma interferon

Vivo, Claire; Levy, F.; Pilatte, Yannick; Fleury‐Feith, Jocelyne; Chrétien, Pascale; Monnet, I.; Kheuang, Laurence; Jaurand, Marie‐Claude

doi:10.1038/sj.onc.1204199

Cited by 26 publications

(16 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although cyclin B1 overexpression plays a crucial role in different tumors, 27 its involvement in mesothelioma, together with p34-cdc2, was demonstrated only in vitro, 28 -30 and a decrease in cell proliferation was associated with reduced cyclin B1/cdc2 activity. 28 We found overexpression of S phase players such as cyclin H (CCNH) and cdc6 transcripts, whereas a G 1 -protein such as cyclin D2 was underexpressed as previously reported in mesothelioma. 31,32 Indeed a G 1 -cyclin-dependent kinase inhibitor p18 (CDKN2C) was overexpressed.…”

mentioning

confidence: 66%

Identification of Potential Therapeutic Targets in Malignant Mesothelioma Using Cell-Cycle Gene Expression Analysis

Romagnoli

Fasoli

Vaira

et al. 2009

The American Journal of Pathology

View full text Add to dashboard Cite

Cell-cycle defects are responsible for cancer onset and growth. We studied the expression profile of 60 genes involved in cell cycle in a series of malignant mesotheliomas (MMs), normal pleural tissues, and MM cell cultures using a quantitative polymerase chain reaction-based, low-density array. Nine genes were significantly deregulated in MMs compared with normal controls. Seven genes were overexpressed in MMs, including the following: CDKN2C, cdc6, cyclin H, cyclin B1, CDC2, FoxM1, and Chk1, whereas Ube1L and cyclin D2 were underexpressed. Chk1 is a principal mediator of cell-cycle checkpoints in response to genotoxic stress. We confirmed the overexpression of Chk1 in an independent set of 87 MMs by immunohistochemistry using tissue microarrays. To determine whether Chk1 down-regulation would affect cell-cycle control and cell survival, we transfected either control or Chk1 siRNA into two mesothelioma cell lines and a nontumorigenic (Met5a)

show abstract

mentioning

confidence: 66%

Identification of Potential Therapeutic Targets in Malignant Mesothelioma Using Cell-Cycle Gene Expression Analysis

Romagnoli

Fasoli

Vaira

et al. 2009

The American Journal of Pathology

View full text Add to dashboard Cite

show abstract

“…The question that then arises is how IFN␥ negatively regulates NP proliferation. One possibility is that IFN␥ induces cell-cycle arrest, an action that has been demonstrated previously in carcinoma cells (Burke et al, 1997;Shyu et al, 2000;Vivo et al, 2001;Baka et al, 2009) and mammalian epithelial cells (Harvat and Jetten, 1996). The anti-proliferative action in these cells is mainly regulated via activation of signal transducer and activator of transcription 1 (STAT1) and downregulation of cyclin A and cyclin E expression (Kortylewski et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Endogenous Interferon Directly Regulates Neural Precursors in the Non-Inflammatory Brain

Li¹,

Walker²,

Zhang³

et al. 2010

Journal of Neuroscience

View full text Add to dashboard Cite

Although a number of growth factors have been shown to be involved in neurogenesis, the role of inflammatory cytokines remains relatively unexplored in the normal brain. Here we investigated the effect of interferon gamma (IFN␥) in the regulation of neural precursor (NP) activity in both the developing and the adult mouse brain. Exogenous IFN␥ inhibited neurosphere formation from the wild-type neonatal and adult subventricular zone (SVZ). More importantly, however, these effects were mirrored in vivo, with mutant mice lacking endogenous IFN␥ displaying enhanced neurogenesis, as demonstrated by an increase in proliferative bromodeoxyuridinelabeled cells in the SVZ and an increased percentage of newborn neurons in the olfactory bulb. Furthermore, NPs isolated from IFN␥ null mice exhibited an increase in self-renewal ability and in the capacity to produce differentiated neurons and oligodendrocytes. These effects resulted from the direct action of IFN␥ on the NPs, as determined by single-cell assays and the fact that nearly all the neurospheres were derived from cells positive for major histocompatibility complex class I antigen, a downstream marker of IFN␥-mediated activation. Moreover, the inhibitory effect was ameliorated in the presence of SVZ-derived microglia, with their removal resulting in almost complete inhibition of NP proliferation. Interestingly, in contrast to the results obtained in the adult, exogenous IFN␥ treatment stimulated neurosphere formation from the embryonic brain, an effect that was mediated by sonic hedgehog. Together these findings provide the first direct evidence that IFN␥ acts as a regulator of the active NP pool in the non-inflammatory brain.

show abstract

“…Two-sided p values of p Ͻ 0.05 or p Ͻ 0.01 were considered statistically significant. (2,3). We demonstrated recently (6) that IGF-I (100 ng/ml) increases the population of total cycling MCF-7 cells (SϩG 2 /M) by 50%.…”

Section: Methodsmentioning

confidence: 99%

“…G 1 phase progression is stimulated by extracellular growth factors (reviewed in Ref. 1), and this progression can be blocked by cytostatic cytokines (2,3). Tumor necrosis factor ␣ (TNF␣) 1 was first identified as a serum-derived substance that causes tumor cell death (4).…”

mentioning

confidence: 99%

Tumor Necrosis Factor α Inhibits Cyclin A Expression and Retinoblastoma Hyperphosphorylation Triggered by Insulin-like Growth Factor-I Induction of New E2F-1 Synthesis

Shen

Yin

Broussard

et al. 2004

Journal of Biological Chemistry

View full text Add to dashboard Cite

Cyclin A is required for cell cycle S phase entry, and its overexpression contributes to tumorigenesis. Release of pre-existing E2Fs from inactive complexes of E2F and hypophosphorylated retinoblastoma (RB) is the prevailing dogma for E2F transcriptional activation of target genes such as cyclin A. Here we explored the hypothesis that new synthesis of E2F-1 is required for insulin-like growth factor-I (IGF-I) to induce cyclin A accumulation and RB hyperphosphorylation, events that are targeted by tumor necrosis factor ␣ (TNF␣) to arrest cell cycle progression. We first established that IGF-I increases expression of cyclin A, causes hyperphosphorylation of RB, and augments the mass of E2F-1 in a time-dependent manner. As expected, E2F-1 small interfering RNA blocks the ability of IGF-I to increase synthesis of E2F-1. Most important, this E2F-1 small interfering RNA also blocks the ability of IGF-I to increase cyclin A accumulation and to hyperphosphorylate RB. We next established that TNF␣ dose-dependently inhibits IGF-I-induced phosphorylation of both RB and histone H1 by cyclin A-dependent cyclin-dependent kinases. Cyclin-dependent kinase 2 (Cdk2) mediates this suppression because co-immunoprecipitation experiments revealed that TNF␣ reduces the amount of IGF-Iinduced cyclin A that binds Cdk2, leading to a reduction in Cdk2 enzymatic activity. TNF␣ antagonizes the ability of IGF-I to increase mass of both E2F-1 and cyclin A but not cyclin E or D1. The cytostatic property of TNF␣ is also shown by its ability to block IGF-I-stimulated luciferase activity of a cyclin A promoter reporter. Deletion of an E2F recognition site from this reporter eliminates the regulatory effects of both IGF-I and TNF␣ on cyclin A transcription, indicating the essential role of E2F-1 in mediating their cross-talk. Collectively, these results establish that TNF␣ targets IGF-I-induced E2F-1 synthesis, leading to inhibition of the subsequent accumulation in cyclin A, formation of cyclin A-Cdk2 complexes, hyperphosphorylation of RB, and cell cycle arrest.

show abstract

Control of cell cycle progression in human mesothelioma cells treated with gamma interferon

Cited by 26 publications

References 44 publications

Identification of Potential Therapeutic Targets in Malignant Mesothelioma Using Cell-Cycle Gene Expression Analysis

Identification of Potential Therapeutic Targets in Malignant Mesothelioma Using Cell-Cycle Gene Expression Analysis

Endogenous Interferon Directly Regulates Neural Precursors in the Non-Inflammatory Brain

Tumor Necrosis Factor α Inhibits Cyclin A Expression and Retinoblastoma Hyperphosphorylation Triggered by Insulin-like Growth Factor-I Induction of New E2F-1 Synthesis

Contact Info

Product

Resources

About