Retinoic acid-induced differentiation of cultured human neuroblastoma cells: a comparison with phorbolester-induced differentiation

Påhlman, Sven; Ruusala, Aino-Inkeri; Abrahamsson, L; Mattsson, Maria; Esscher, T

doi:10.1016/0045-6039(84)90038-1

Cited by 521 publications

(372 citation statements)

References 11 publications

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“…Since Notch signalling is important during the embryonal development of the SNS, where it inhibits neuronal differentiation to take place prematurely, it seems likely that any dysregulated activity of this cascade would contribute to maintaining the cells in an undifferentiated, proliferating stage. Neuroblastoma represents an almost unique tumour cell type in its capacity to differentiate upon treatment with different types of inducing agents, upregulating a well-established set of differentiation marker genes, making it possible to monitor the differentiation process (Påhlman et al, 1984(Påhlman et al, , 1991Bjelfman et al, 1990). We have previously shown that most NB cell lines express Hash-1 and that the expression of Hes-1 is transiently increased upon induced differentiation with a concomitant decrease in Hash-1 expression (Grynfeld et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Effects of the histone deacetylase inhibitor valproic acid on Notch signalling in human neuroblastoma cells

et al. 2005

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Neuroblastoma (NB), a sympathetically derived childhood tumour, shows characteristics of neuronal precursor cells, suggesting a halted differentiation process. We have previously shown that the Notch signalling cascade, a key player during normal neurogenesis, also might be involved in NB differentiation. Valproic acid (VPA), a well-tolerated antiepileptic drug, has been shown to induce differentiation and cell death of NB cells, possibly associated with its recently described HDAC inhibiting activity. Stimulation of NB cells with VPA led to increased cell death and phenotypic changes associated with differentiation, that is, neurite extension and upregulation of neuronal markers. VPA treatment also led to an activated Notch signalling cascade as shown by increased levels of intracellular Notch-1 and Hes-1, mimicking the initial phase of induced differentiation. These results reinforce that VPA potentially could be used in differentiation therapy of NB and that the effects in part could be a consequence of interference with the Notch signalling cascade.

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Section: Discussionmentioning

confidence: 99%

Effects of the histone deacetylase inhibitor valproic acid on Notch signalling in human neuroblastoma cells

et al. 2005

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“…6, 3), as reported previously. 17,19,20 Cells stimulated with the combination of RAϩIFN-␥ differed from both RA and IFN-␥-stimulated cells; they were often large, spread out, flattened cells, in contrast to the smaller RA-differentiated cells, and extended rather thick and less branched processes compared to the IFN-␥-treated cells (Fig. 6b-d).…”

Section: Ifn-␥ Cooperates With Ra and Tpa To Induce Differentiation Omentioning

confidence: 99%

Interferon-? cooperates with retinoic acid and phorbol ester to induce differentiation and growth inhibition of human neuroblastoma cells

et al. 2001

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The prognosis of patients with advanced stages of neuroblastoma with N-myc amplification remains poor despite escalated therapy, a situation that has called for alternative therapeutic approaches. Neuroblastoma cells, which represent immature peripheral neuronal cells, treated with certain physiologic and nonphysiologic agents such as retinoic acid (RA), phorbol esters and interferons (IFN) in vitro undergo cellular differentiation and stop to divide, a process that mimics normal neuronal development. Such "differentiation therapy" using RA after autologous bone marrow transplantation has recently given encouraging results in neuroblastoma patients with advanced disease. Considering approaches for improved differentiation therapy, we investi-

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“…1,[9][10][11] Retinoids act on upregulating diverse sets of differentiationrelated gene expression via retinoic acid receptors (RAR and RXR) such as GAP43 and neurotrophin receptors (TrK). [12][13][14] In addition, retinoids can also downregulate the expression of certain genes such as N-MYC, concurrent with the arrest of cell proliferation. 11,5,16 Elucidating the mechanisms behind the differentiation of neuroblastoma cells is therefore of clinical importance.…”

Section: Introductionmentioning

confidence: 99%

Deubiquitinating activity of CYLD is impaired by SUMOylation in neuroblastoma cells

2014

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CYLD is a deubiquitinating (DUB) enzyme that has a pivotal role in modulating nuclear factor kappa B (NF-κB) signaling pathways by removing the lysine 63-and linear-linked ubiquitin chain from substrates such as tumor necrosis factor receptor-associated factor 2 (TRAF2) and TRAF6. Loss of CYLD activity is associated with tumorigenicity, and levels of CYLD are lost or downregulated in different types of human tumors. In the present study, we found that high CYLD expression was associated with better overall survival and relapse-free neuroblastoma patient outcome, as well as inversely correlated with the stage of neuroblastoma. Retinoic acid-mediated differentiation of neuroblastoma restored CYLD expression and promoted SUMOylation of CYLD. This posttranslational modification inhibited deubiquitinase activity of CYLD against TRAF2 and TRAF6 and facilitated NF-κB signaling. Overexpression of non-SUMOylatable mutant CYLD in neuroblastoma cells reduced retinoic acid-induced NF-κB activation and differentiation of cells, but instead promoted cell death.

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Retinoic acid-induced differentiation of cultured human neuroblastoma cells: a comparison with phorbolester-induced differentiation

Cited by 521 publications

References 11 publications

Effects of the histone deacetylase inhibitor valproic acid on Notch signalling in human neuroblastoma cells

Effects of the histone deacetylase inhibitor valproic acid on Notch signalling in human neuroblastoma cells

Interferon-? cooperates with retinoic acid and phorbol ester to induce differentiation and growth inhibition of human neuroblastoma cells

Deubiquitinating activity of CYLD is impaired by SUMOylation in neuroblastoma cells

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