Noradrenaline inhibits the programmed cell death induced by 1,25-dihydroxyvitamin D3 in glioma

Canova, Cécile; Baudet, Christian; Chevalier, G.; Brachet, Philippe; Wion, Didier

doi:10.1016/s0014-2999(96)00942-9

Cited by 13 publications

(7 citation statements)

References 13 publications

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“…Treatment with the β adrenergic agonist isoproterenol dose-dependently enhances U251MG glioblastoma cellular proliferation by promoting the phosphorylation and enzymatic activity of ERK1/2 in vitro [67]. Norepinephrine reduces cellular proliferation and uptake of l-arginine in rat glial cells [68] and 1,25-dihydroxycholecalciferolinduced apoptosis of glioma cells in vitro [69]. The bitopic compound ( , ' )-fenoterol inhibits proliferation of, and reduces l-arginine uptake in, N1321 astrocytoma and U118 glioblastoma cells [9].…”

Section: Modulation Of Cellular Proliferation By β Adrenergic Signalingmentioning

confidence: 99%

RETRACTED ARTICLE: β adrenergic receptor modulated signaling in glioma models: promoting β adrenergic receptor-β arrestin scaffold-mediated activation of extracellular-regulated kinase 1/2 may prove to be a panacea in the treatment of intracranial and spinal malignancy and extra-neuraxial carcinoma

Ghali

2020

Mol Biol Rep

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Neoplastically transformed astrocytes express functionally active cell surface β adrenergic receptors (βARs). Treatment of glioma models in vitro and in vivo with β adrenergic agonists variably amplifies or attenuates cellular proliferation. In the majority of in vivo models, β adrenergic agonists generally reduce cellular proliferation. However, treatment with β adrenergic agonists consistently reduces tumor cell invasive potential, angiogenesis, and metastasis. β adrenergic agonists induced decreases of invasive potential are chiefly mediated through reductions in the expression of matrix metalloproteinases types 2 and 9. Treatment with β adrenergic agonists also clearly reduce tumoral neoangiogenesis, which may represent a putatively useful mechanism to adjuvantly amplify the effects of bevacizumab. Bevacizumab is a monoclonal antibody targeting the vascular endothelial growth factor receptor. We may accordingly designate βagonists to represent an enhancer of bevacizumab. The antiangiogenic effects of β adrenergic agonists may thus effectively render an otherwise borderline effective therapy to generate significant enhancement in clinical outcomes. β adrenergic agonists upregulate expression of the major histocompatibility class II DR alpha gene, effectively potentiating the immunogenicity of tumor cells to tumor surveillance mechanisms. Authors have also demonstrated crossmodal modulation of signaling events downstream from the β adrenergic cell surface receptor and microtubular polymerization and depolymerization. Complex effects and desensitization mechanisms of the β adrenergic signaling may putatively represent promising therapeutic targets. Constant stimulation of the β adrenergic receptor induces its phosphorylation by β adrenergic receptor kinase (βARK), rendering it a suitable substrate for alternate binding by β arrestins 1 or 2. The binding of a β arrestin to βARK phosphorylated βAR promotes receptor mediated internalization and downregulation of cell surface receptor and contemporaneously generates a cell surface scaffold at the βAR. The scaffold mediated activation of extracellular regulated kinase 1/2, compared with protein kinase A mediated activation, preferentially favors cytosolic retention of ERK1/2 and blunting of nuclear translocation and ensuant pro-transcriptional activity. Thus, βAR desensitization and consequent scaffold assembly effectively retains the cytosolic homeostatic functions of ERK1/2 while inhibiting its pro-proliferative effects. We suggest these mechanisms specifically will prove quite promising in developing primary and adjuvant therapies mitigating glioma growth, angiogenesis, invasive potential, and angiogenesis. We suggest generating compounds and targeted mutations of the β adrenergic receptor favoring β arrestin binding and scaffold facilitated activation of ERK1/2 may hold potential promise and therapeutic benefit in adjuvantly treating most or all cancers. We hope our discussion will generate fruitful research endeavors seeking to exploit these mechanisms.

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Section: Modulation Of Cellular Proliferation By β Adrenergic Signalingmentioning

confidence: 99%

RETRACTED ARTICLE: β adrenergic receptor modulated signaling in glioma models: promoting β adrenergic receptor-β arrestin scaffold-mediated activation of extracellular-regulated kinase 1/2 may prove to be a panacea in the treatment of intracranial and spinal malignancy and extra-neuraxial carcinoma

Ghali

2020

Mol Biol Rep

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“…It is well known that catecholamines stimulate the growth of neonatal (Simpson et al, 1982;Bogoyevitch et al, 1996) and adult (Pinson et al, 1993) cardiac myocytes. Recently, both norepinephrine and isoproterenol were also found to protect brown adipocytes (Lindquist and Rehnmark, 1998), hepatocytes (Zhang et al, 1996), glioma cells (Canova et al, 1997), and neonatal cardiac myocytes (Wu et al, 1997) against apoptotic death. In the latter study, 1 M norepinephrine prevented neonatal cardiac myocytes from atrial natriuretic peptide-induced apoptosis through the activation of ␤-adrenoceptors and an increase in the intracellular cAMP concentration (Wu et al, 1997) but the precise molecular targets of cyclic nucleotide-modulated cell fate decision remained unknown.…”

Section: Discussionmentioning

confidence: 99%

Low Catecholamine Concentrations Protect Adult Rat Ventricular Myocytes against Apoptosis through cAMP-Dependent Extracellular Signal-Regulated Kinase Activation

2000

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Catecholamines have complex effects on cardiac myocyte growth and survival, including the triggering of apoptosis at high concentration. Here, we examined whether at a lower concentration, catecholamine protected adult rat ventricular myocytes from apoptosis in vitro. Myocytes were exposed to staurosporine (ST, 10 microM) for 18 h, with or without epinephrine (0.1 or 10 microM) or fetal calf serum (10%). Apoptosis was assessed after 48 h of culture in terms of DNA fragmentation (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling method, DNA gel electrophoresis). Epinephrine (0.1 microM) and serum reduced ST-induced myocyte apoptosis by approximately 50% (n = 12 cultures, P <.001), whereas epinephrine and serum alone did not influence the low apoptotic rate in control cultures. In contrast, 10 microM epinephrine induced marked apoptosis in ST-free conditions. The protective effects of 0.1 microM epinephrine and serum were blunted by the tyrosine kinase inhibitor genistein (n = 12 cultures, P <. 001). Extracellular signal-regulated kinase (ERK) activity was stimulated by 0.1 microM epinephrine but not by 10 microM epinephrine. Furthermore, the protective effect of epinephrine was mimicked by isoproterenol (1 microM) and forskolin (1 microM) but not by phenylephrine (10 microM) and was blunted by propranolol (10 microM) but not by prazozin (10 microM). Finally, isoproterenol and forskolin activated ERK, an effect that was blunted by propranolol. In conclusion, low epinephrine concentrations attenuate ST-induced apoptosis of adult cardiac myocytes in vitro, an effect mediated by coupling between the cAMP pathway and ERK activation. This suggests that a minimal adrenergic tone is essential for myocyte survival in conditions of unusual stress.

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“…However, further studies in the rat glioma cell line C6.9 showed that noradrenaline and the beta-adrenoceptor agonist isoproterenol inhibited 1,25(OH) 2 D 3 -induced apoptosis and that the beta-adrenoceptor antagonist propanolol reversed this inhibition. These findings suggest that the efficiency of antiproliferative vitamin D-related therapies could be influenced by endogenous levels of noradrenaline (32). Furthermore, changes in the DNA methylation pattern could suppress 1,25(OH) 2 D 3 -mediated apoptosis via expression of hypermethylated genes, such as proto- oncogenes, with death-repressor activity (33).…”

Section: Vitaminsmentioning

confidence: 99%

Modulation of Glioma Risk and Progression by Dietary Nutrients and Antiinflammatory Agents

2011

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Gliomas are tumors of glial origin formed in the central nervous system and exhibit profound morphological and genetic heterogeneity. The etiology of this heterogeneity involves an interaction between genetic alterations and environmental risk factors. Scientific evidence suggests that certain natural dietary components, such as phytoestrogens, flavonoids, polyunsaturated fatty acids and vitamins may exert a protective effect against gliomas by changing the nature of the interaction between genetics and environment. Similarly, certain anti-inflammatory drugs and dietary modifications, such as methionine restriction and the adoption of low-calorie or ketogenic diets, may take advantage of glioma and normal glial cells’ differential requirements for glucose, methionine, and ketone bodies and may therefore be effective as part of preventive or treatment strategies for gliomas. Treatment trials of glioma patients and chemoprevention trials of individuals with a known genetic predisposition to glioma using the most promising of these agents, such as the anti-inflammatory drugs curcumin and gamma-linolenic acid, are needed to validate or refute these agents’ putative role in gliomas.

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Noradrenaline inhibits the programmed cell death induced by 1,25-dihydroxyvitamin D3 in glioma

Cited by 13 publications

References 13 publications

Low Catecholamine Concentrations Protect Adult Rat Ventricular Myocytes against Apoptosis through cAMP-Dependent Extracellular Signal-Regulated Kinase Activation

Modulation of Glioma Risk and Progression by Dietary Nutrients and Antiinflammatory Agents

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