Phosphatidylinositol turnover is not a general regulator of neuroblastoma cell differentiation: comparison between two differentiating agents, retinoic acid and γ‐interferon

Lanciotti, Marina; Cornaglia-Ferraris, P.; Ponzoni, Mirco

doi:10.1016/0014-5793(89)80146-2

Cited by 7 publications

(3 citation statements)

References 27 publications

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“…The kinetics of accumulation of cAMP indicates that, although this accumulation occurred prior to the detectable increase in expression of ICAM-1, stimulation of the CAMP-dependent transduction pathway by retinoic acid is not an early event and suggests the involvement of other second messengers. The demonstrated ability of retinoids to stimulate protein kinase C and phospholipase C in various systems may be of relevance in this respect (Isakov, 1988;Niles and Loewy, 1989;Lanciotti et al, 1989;Pailler-Rodde et al, 1991).…”

Section: Discussionmentioning

confidence: 99%

Biphasic effect of camp‐elevating agents on ICAM‐1 expression stimulated by retinoic acid and interferonγ

Bouillon

Fortier

Boulianne

et al. 1992

Intl Journal of Cancer

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Incubation of the human glioma cell line HS 683 in the presence of IFN-gamma or retinoic acid strongly stimulates the cell-surface expression of the intercellular adhesion molecule ICAM-1. We have investigated the role of the cAMP-mediated signal transduction pathway in this process and report that pharmacological agents which increased the intracellular levels of cAMP exhibited a biphasic action on ICAM-1 expression in human glioma cell line HS 683. Treatment for 1 hr with 25 microM forskolin or 1 mM isobutylmethylxanthine, or for 12 hr with 100 ng/ml pertussis toxin or 50 micrograms/ml cholera toxin transiently stimulated ICAM-1 expression with a maximal level of expression 8 hr post treatment, after which time ICAM-1 expression returned to the basal level. On the other hand, such pretreatments inhibited the inducing effects of either retinoic acid or IFN-gamma. Indeed, 24 hr after treatment with cAMP-elevating agents, both the retinoic-acid- and the IFN-gamma-induced ICAM-1 expression were inhibited by 60 to 80%, with a maximal 90 to 100% inhibition 72 hr post treatment. This inhibition of the cell-surface expression of ICAM-1 was confirmed at the mRNA level. The intracytoplasmic levels of cAMP were also quantified following treatments with forskolin, retinoic acid or IFN-gamma. In response to forskolin, cAMP levels increased 30-fold within 5 min, whereas a 10-fold increase occurred 60 min following treatment with 10 microM retinoic acid. Interferon gamma, in contrast, did not induce cAMP accumulation. These results were also correlated with an in vitro activation of adenylyl cyclase activity by retinoic acid and inhibition of this activity by IFN-gamma, in a dose-dependent and a GTP-dependent manner. Our results suggest that the suppression of IFN-gamma-induced ICAM-1 expression, obtained upon pre-treatment with cAMP-elevating agents, is due to direct antagonism with IFN-gamma action on adenylyl cyclase. However, the inhibition of retinoic-acid-induced ICAM-1 expression cannot be explained by the same mechanisms. The timing of adenylyl cyclase stimulation and cAMP accumulation, as well as the levels of cAMP accumulation, are probably involved in this inhibition. Our results also emphasize the fact that the induction of ICAM-1 expression is a multi-step process implicating different transductional signals among which cAMP might be involved as a second messenger.

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Section: Discussionmentioning

confidence: 99%

Biphasic effect of camp‐elevating agents on ICAM‐1 expression stimulated by retinoic acid and interferonγ

Bouillon

Fortier

Boulianne

et al. 1992

Intl Journal of Cancer

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“…The results in A are representative of five independent experiments, and those in B represent three independent experiments each done in duplicate ('P< 0.05; "'P<0.001, evaluated by Student's t-test for unpaired data).indicating a constitutive activation of PLA2 in our model as well as an increase in AA metabolism in response to IFN-~,. The possibility of an AA release by phospholipase C activation and subsequent deacylation of diacylglyceroi in response to IFN-7 has been previously ruled out[20].Further evidence of PLA2 activation in response to IFN.-?" was obtained by measuring [3H]AA release in LAN-5 cells treated with subsaturating amounts of IFN-?"…”

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confidence: 99%

Stimulation of receptor‐coupled phospholipase A₂ by interferon‐γ

1992

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The biomolecular mechanisms that mediate signal transduction by type 11 (γ) interferon (IFN) are poorly understood. IFN‐γ is a potent growth inhibitory cytokine also endowed with antiviral, immunomodulatory, and differentiating activities on various cell targets, including neural cells. IFN‐γ induced a rapid and transient activation of phospholipase A2 in LAN‐5, a human neuroblastoma cell line. A consequence of phospholipase A2 activation was the release of arachidonic acid and the generation of lysophospholipids from membrane phospholipids. Treatment of pre‐labeled LAN‐5 cells with a receptor‐saturating concentration of IFN‐γ led to a time‐dependent release of [3H]arachidonic acid into the culture media and generation or [32P]lysophosphatidylcholine. Pretreatment of cultures with the phospholipase A2 inhibitor, bromophenacyl bromide, markedly inhibited both [3H]arachidonic acid release and lysophosphatidylcholine production induced by IFN‐γ treatment. Pretreatment of LAN‐5 cells with nordihydroguaiaretic acid, a lipoxygenase inhibitor, or with indomethacin, a cyclooxygenase inhibitor, amplified the release of[3H]arachidonic acid and production of lysophosphatidylcholine induced by non‐saturating concentrations of IFN‐γ. In parallel, and with the same time‐dependent effect, a significant decrease in phosphatidylcholine labeling was observed in IFN‐γ‐treated cells, further indicating that a potential signal transduction mechanism of IFN‐γ is the hydrolysis of membrane phosphatidylcholine by phospholipase A2.

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“…However, some clinical exceptions have been described (13,14). Continuous human NB cell lines have become important in vitro models for this type of tumor (9,10,15,16). A biologic classification of cell lines derived from human extracranial neural tumors has been recently proposed (17).…”

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confidence: 99%

A New Human Highly Tumorigenic Neuroblastoma Cell Line with Undetectable Expression of N-myc

et al. 1990

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ABSTRACT. A peculiar human cell line (GI-ME-N) derived from the metastatic bone marrow of a Zyr-old patient with stage IV neuroblastoma (NB) was extensively characterized. Cell-type-specific markers, tumorigenicity in nude mice, morphology, cytogenetics, and amplification/ expression of the N-myc gene were evaluated. All metaphases presented the typical l p deletion. Surface markers specific for NB cells, vimentin, and neurofilament proteins were all clearly detectable with immunofluorescence and/ or western blot procedures. Moreover, it was found that GI-ME-N cells did not express N-myc oncogene or HLA class 1 antigens, and were not classified as peripheral neuroectodermal tumor cells. However, extremely short latency and survival times, comparable to peripheral neuroectodermal tumor cells, were observed in nude mice grafted with GI-ME-N. In addition, no correlations were. observed in tumorigenicity of N-myc amplified (IMR32) versus unamplified (SK-N-SH GI-ME-N) human NB cell lines in nude mice. We conclude that N-myc amplification/ expression do not correlate with the aggressiveness of human NB in athymic animals, which is not always explained by the peripheral neuroectodermal tumor cell nature of the malignant cells, either. (Pediatr Res 27: 1-6, 1990) Abbreviations NB, neuroblastoma GI-ME-N, Gaslini Institute, patient initials, neuroblastoma PNET, peripheral neuroectodermal tumor BM, bone marrow s.c., subcutaneous Neuroblastoma, a neoplasm of the sympathetic nervous system, is the most common extracranial solid tumor arising in children (1, 2). In contrast to other pediatric tumors, the prognosis of NB patients has not significantly improved in the last 10 yr. With conventional chemotherapy, including local irradi-

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Phosphatidylinositol turnover is not a general regulator of neuroblastoma cell differentiation: comparison between two differentiating agents, retinoic acid and γ‐interferon

Cited by 7 publications

References 27 publications

Biphasic effect of camp‐elevating agents on ICAM‐1 expression stimulated by retinoic acid and interferonγ

Biphasic effect of camp‐elevating agents on ICAM‐1 expression stimulated by retinoic acid and interferonγ

Stimulation of receptor‐coupled phospholipase A₂ by interferon‐γ

A New Human Highly Tumorigenic Neuroblastoma Cell Line with Undetectable Expression of N-myc

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Phosphatidylinositol turnover is not a general regulator of neuroblastoma cell differentiation: comparison between two differentiating agents, retinoic acid and γ‐interferon

Cited by 7 publications

References 27 publications

Biphasic effect of camp‐elevating agents on ICAM‐1 expression stimulated by retinoic acid and interferonγ

Biphasic effect of camp‐elevating agents on ICAM‐1 expression stimulated by retinoic acid and interferonγ

Stimulation of receptor‐coupled phospholipase A2 by interferon‐γ

A New Human Highly Tumorigenic Neuroblastoma Cell Line with Undetectable Expression of N-myc

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Stimulation of receptor‐coupled phospholipase A₂ by interferon‐γ