Haemopoietic colony stimulating factors promote cell survival by suppressing apoptosis

Williams, Gwyn T.; Smith, Christopher A.; Spooncer, Elaine; Dexter, T. M.; Taylor, D.L.

doi:10.1038/343076a0

Cited by 879 publications

(392 citation statements)

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“…For instance, the enhancement of cell survival actively suppressing the process of apoptosis is distinct from the stimulation of proliferation. 3 For the purpose of convenience, the cytokines and the cell lines are arranged in Table 2 in alphabetical order (and not according to common functional aspects of the cytokines or their receptors or to a common origin of the cell lines). Examples of detailed cytokine response profiles are given for the well-known and most often used growth factor-dependent cell lines, namely M-07e and TF-1 (Figure 2).…”

Section: +10%mentioning

confidence: 99%

“…This rapid cell death occurs by an active cellular ietic cells presents difficulties for the identification of cytoprocess (apoptosis) that can be suppressed by new addition kines with specific effects on certain types of cells and at the of growth factors. 3 Most of these cell lines showed a growth various stages of activation, proliferation or differentiation.…”

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Cytokine response profiles of human myeloid factor-dependent leukemia cell lines

1997

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Cytokine response profiles of human myeloid factor-dependent leukemia cell lines

1997

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“…DNA damage) further supports this view. Moreover, it has been reported that differentiated haematopoietic cells are less prone to apoptotic death than their undifferentiated precursors (Williams et al, 1990). In this scenario, it might be speculated that forced expression of wt-p53 normalizes the cellular functions of leukaemia cells and allows them to respond to intracellular signals, which drive the cell to apoptosis or differentiation.…”

Section: Discussionmentioning

confidence: 99%

Wt-p53 action in human leukaemia cell lines corresponding to different stages of differentiation

Rizzo¹,

Zepparoni²,

Cristofanelli³

et al. 1998

Br J Cancer

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Summary Recent studies support the potential application of the wt-p53 gene in cancer therapy. Expression of exogenous wt-p53 suppresses a variety of leukaemia phenotypes by acting on cell survival, proliferation and/or differentiation. As for tumour gene therapy, the final fate of the neoplastic cells is one of the most relevant points. We examined the effects of exogenous wt-p53 gene expression in several leukaemia cell lines to identify p53-responsive leukaemia. The temperature-sensitive p53vallw mutant or the human wt-p53 cDNA was transduced in leukaemia cell lines representative of different acute leukaemia FAB subtypes, including Ml (Ozturk et al, 1992;Gotz and Montenarh 1995). Therefore, the identification of leukaemia cells susceptible to wt-p53-induced apoptosis should be useful for therapeutic purposes. In spite of the evidence that cellular context determines the final outcome of the cells after wt-p53 forced expression (Canman et al, 1995;Soddu et al, 1996), it is still unclear how to classify the cellular environments as a function of the response to wt-p53 action. In this respect, we asked whether the stage of differentiation might be a good parameter to classify the final outcome of wt-p53-transduced leukaemia cells. To address this question, seven leukaemia cell lines were transfected with a temperature-sensitive p53 (tsp53)-encoding vector or infected with a wt-p53 recombinant retrovirus. Viral infection was used in addition to plasmid transfection to evaluate the feasibility of a gene therapy approach based on wt-p53 expression in leukaemia cells. Leukaemia heat-inactivated fetal bovine serum (FBS). The Psi-2 crip-ampho (Markowitz et al, 1988) amphotropic packaging cells were cultured in Dulbecco's modified Eagle medium (DMEM) supplemented with 10% FBS. The plasmids pN53cG , carrying the ts-pS3Va-13S mutant gene (Soddu et al, 1994), and pRSVneo, carrying the selectable marker for G418 resistance, were used. The pLp53SN vector was obtained by inserting the human wt-p53 cDNA (Baker et al, 1990) into the unique BamHI site of pLXSN vectors (Miller and Rosman, 1989). Transfections and infectionsAfter 10 min incubation on ice, HEL 92.1.7, U937 and K562 cells [5 x 106 in 0.3 ml of phosphate-buffered saline (PBS)] were electroporated (HEL 92.1.7: 0.25 kV, 960 [F; U937 and K562: 0.2 kV, 960 tF) with 10 gg of plasmid, incubated for an additional 10 min on ice and plated in complete medium. G418 was added after 48 h (HEL 92.1.7: 1 mg ml-'; U937 and K562: 750 gg ml-'). HL-60 cells transfected with pN53cG(Val-135) (HL-2) and with

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“…The observation that withdrawal of IL-3 from progenitor cell lines or primary IL-3 dependent bone marrow derived cells resulted in apoptosis of these cells (Collins et al, 1992;Williams et al, 1990) indicates anti-apoptosis activity of IL-3 in hematopoietic cells. Our analysis of the anti depletion-induced apoptosis activity of GM-CSF in mouse IL-3 dependent BA/F3 cells (Palacios and Steinmetz, 1985) showed the same requirement of the bc region as for proliferation promotion (Liu et al, 1999b,c).…”

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confidence: 99%

Analysis of mechanisms involved in the prevention of γ irradiation-induced apoptosis by hGM-CSF

Liu

Mohi

et al. 2000

Oncogene

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Human granulocyte-macrophage colony-stimulating factor (hGM-CSF) induces proliferation and sustains viability of the mouse interleukin (IL)-3 dependent lymphoid cell line BA/F3 expressing the hGM-CSF receptor. Caspase-3 like enzyme activity and DNA fragmentation were augmented by depletion of this factor from the cell, and exposure to g irradiation accelerated kinetics of these events. Anti g irradiationinduced apoptosis occurred through various mutant GM-CSF receptors and only the box1 region was essential while the C terminal region, including tyrosine residues which are required for MAPK cascade activation, was dispensable. Consistent with this notion, the addition of PD98059 had no e ect on this activity thereby indicating that activation of MAPK is not essential for the activity. As expected, g irradiation increased p53 protein and bax mRNA levels and the presence of hGM-CSF dramatically modulated bax/bcl-X L ratio. The PI-3K speci®c inhibitor wortmannin did not a ect hGM-CSF dependent anti g irradiation induced apoptosis nor bcl-X L induction, thus bcl-X L but not PI-3K pathway seems to be involved in hGM-CSF dependent anti g irradiation-induced apoptosis. It is well documented that the box1 region is essential for GM-CSF dependent activation of JAK2 and JAK2 speci®c inhibitor AG490 suppressed anti g irradiation-induced apoptosis by hGM-CSF. An arti®cial JAK2 activating molecule in which extracellular and the transmembrane of bc fused with whole JAK2 can sustain BA/F3 cells survival and proliferation mIL-3 independently, but these cells are susceptible to g irradiation. Furthermore GyrB/Jak2, which can activate STAT5 but not the MAPK cascade nor survival of BA/F3 cells, also could not prevent g irradiation-induced apoptosis. Although JAK2 is essential for hGM-CSF dependent anti g irradiation-induced apoptosis, it appeared that JAK2 does not seem su cient for the activity. Oncogene (2000) 19, 571 ± 579.

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Haemopoietic colony stimulating factors promote cell survival by suppressing apoptosis

Cited by 879 publications

References 24 publications

Cytokine response profiles of human myeloid factor-dependent leukemia cell lines

Cytokine response profiles of human myeloid factor-dependent leukemia cell lines

Wt-p53 action in human leukaemia cell lines corresponding to different stages of differentiation

Analysis of mechanisms involved in the prevention of γ irradiation-induced apoptosis by hGM-CSF

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