The effects of serum depletion and dexamethasone on growth and differentiation of human neuroblastoma cell lines

Glick, Richard D.; Medary, Irene; Aronson, Daniël C.; Scotto, Kathleen W.; Swendeman, Steven; Quaglia, Michael P. La

doi:10.1016/s0022-3468(00)90216-1

Cited by 25 publications

(20 citation statements)

References 20 publications

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“…Studies in a variety of cell lines in vitro have indicated that antiproliferative effects of GCs may be mediated by a reversible G 1 -block in cell cycle progression [42][43][44] since after withdrawal of corticosteroids cells synchronously progressed through the cell cycle. 44,45 Investigations with glioblastoma cells, 46 osteosarcoma cells 40 and ovarian cancer cells, 41 have shown that DEX led to cell growth arrest in a time-and dose-dependent manner.…”

Section: Effect Of Gcs On Cell Proliferation and Cell Cycle Progressionmentioning

confidence: 99%

Cell Cycle Arrest by Glucocorticoids May Protect Normal Tissue and Solid Tumors from Cancer Therapy

Mattern¹,

Büchler²,

Herr³

2007

Cancer Biology & Therapy

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ABBrevIAtIons DEX ABstrActGlucocorticoids have been widely used as cotreatment for patients with cancer due to potent pro-apoptotic properties in lymphoid cells, reduction of nausea and diminishing acute toxicity on normal tissue. There are now data from preclinical and, to some extent, clinical studies, demonstrating that these medicaments are highly suspicious to induce therapy resistance in the majority of malignant solid tumors-irrespective of tumor origin and the nature of specific anticancer drugs or irradiation used for treatment. Despite these huge amounts of data, the underlying mechanisms of cell type-specific signaling by these steroid hormones are just beginning to be described. This review summarizes our present understanding of a relationship between glucocorticoid-induced reversible cell cycle arrest and therapy resistance in solid tumors. We give a summary of our current knowledge of decreased proliferation rates in response to glucocorticoid pre and combination treatment which are suspicious to be involved not only in protection of normal tissues, but also in protection of solid tumors from cytotoxic effects of anticancer agents. The inhibition of cell cycle progression by pretreatment with GCs may be crucially involved in switching the balance of several interacting pathways to survival upon treatment with GCs.

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Section: Effect Of Gcs On Cell Proliferation and Cell Cycle Progressionmentioning

confidence: 99%

Cell Cycle Arrest by Glucocorticoids May Protect Normal Tissue and Solid Tumors from Cancer Therapy

Mattern¹,

Büchler²,

Herr³

2007

Cancer Biology & Therapy

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“…Since the cytoskeleton provides "a structural framework around which cell shape and polarity are defined" (37) it is tempting to conclude that changes in the cytoskeleton organization are involved in the modification of the cell migration induced by Dex. On the other hand, it has been reported that Gc induce morphological changes of neuroblastoma cells (6,7,14). The results reported here showing that Dex treatment brings about a transdifferentiation of SK-N-SH cells that shift from the neurallike to the epithelial-like phenotype seem to confirm these findings.…”

Section: Discussionmentioning

confidence: 99%

“…The differentiation of sympathoadrenal precursor cells may proceed towards either sympathetic neurons or chromaffin cells; these changes may be induced by several factors and hormones. Neuroblastoma cells have been consequently utilized as a model to analyze the effects of the endocrine milieu on the differentiation of sympathoadrenal cells (6,7,9,10).…”

Section: La Casulari Et Almentioning

confidence: 99%

“…26) which are involved in essential biological processes such as growth, development, metabolism, behavior, and apoptosis. Only one report has been published so far indicating, on the basis of Western blot analysis, that GR are present in several neuroblastoma cell lines (6). No study has been devoted to the analysis of the binding characteristics of GR present in neuroblastoma cells.…”

Section: La Casulari Et Almentioning

confidence: 99%

“…Differentiation of the cells derived from the neural crest is strongly influenced by the endocrine environment (1)(2)(3)(4)(5)(6)(7). The study of the influence of hormones on cell differentiation was facilitated after different cell lines were isolated from tumors derived from cells originating in the neural crest (neuroblastomas, pheochromocytomas).…”

Section: Introductionmentioning

confidence: 99%

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Dexamethasone blocks the migration of the human neuroblastoma cell line SK-N-SH

Casulari¹,

Dondi²,

Maggi³

et al. 2006

Braz J Med Biol Res

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Glucocorticoids (Gc) influence the differentiation of neural crestderived cells such as those composing sympathoadrenal tumors like pheochromocytomas, as well as neuroblastomas and gangliomas. In order to obtain further information on the effects of Gc on cells evolving from the neural crest, we have used the human neuroblastoma cell line SK-N-SH to analyze: 1) the presence and the binding characteristics of Gc receptors in these cells, 2) the effect of dexamethasone (Dex) on the migration of SK-N-SH cells, and 3) the effect of Dex on the organization of the cytoskeleton of SK-N-SH cells. We show that: 1) receptors that bind [ 3 H]-Dex with high affinity and high capacity (Kd of 9.6 nM, Bmax of 47 fmol/mg cytosolic protein, corresponding to 28,303 sites/cell) are present in cytosolic preparations of SK-N-SH cells, and 2) treatment with Dex (in the range of 10 nM to 1 µM) has an inhibitory effect (from 100% to 74 and 43%, respectively) on the chemotaxis of SK-N-SH cells elicited by fetal bovine serum. This inhibition is completely reversed by the Gc receptor antagonist RU486 (1 µM), and 3) as demonstrated by fluorescent phalloidin-actin detection, the effect of Dex (100 nM) on SK-N-SH cell migration is accompanied by modifications of the cytoskeleton organization that appear with stress fibers. These modifications did not take place in the presence of 1 µM RU486. The present data demonstrate for the first time that Dex affects the migration of neuroblastoma cells as well as their cytoskeleton organization by interacting with specific receptors. These findings provide new insights on the mechanism(s) of action of Gc on cells originating in the neural crest.

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Dexamethasone affects mouse olfactory mucosa gene expression and attenuates genes related to neurite outgrowth

Tian

Pinto

et al. 2015

Int Forum Allergy Rhinol

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The effects of serum depletion and dexamethasone on growth and differentiation of human neuroblastoma cell lines

Cited by 25 publications

References 20 publications

Cell Cycle Arrest by Glucocorticoids May Protect Normal Tissue and Solid Tumors from Cancer Therapy

Cell Cycle Arrest by Glucocorticoids May Protect Normal Tissue and Solid Tumors from Cancer Therapy

Dexamethasone blocks the migration of the human neuroblastoma cell line SK-N-SH

Dexamethasone affects mouse olfactory mucosa gene expression and attenuates genes related to neurite outgrowth

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