Effects of epidermal growth factor on the [3H]-thymidine uptake in the SK-N-SH and SH-SY5Y human neuroblastoma cell lines

Abstract

The studies on the factors that regulate the biology of the neuroblastoma cell lines may offer important information on the development of tissues and organs that derive from the neural crest. In the present paper we study the action of epidermal growth factor (EGF) on two human neuroblastoma cell lines: SK-N-SH which is composed at least of two cellular phenotypes (neuroblastic and melanocytic/glial cells), and its pure neuroblastic subclone SH-SY5Y. The results show that EGF (10 ng/ml) significantly stimulates the incorporation of [3H]-thymidine in the SK-N-SH cells only in the presence of fetal bovine serum (FBS) (control = 58,285 +/- 9327 cpm; EGF = 75,523 +/- 4457, p < 0.05). Such effect is not observed in the presence of a chemical defined medium, that is, in the absence of FBS (control = 100,997 +/- 4375; EGF = 95,268 +/- 4683; NS) In the SH-SY5Y cells the EGF does not modify the incorporation of [3H]-thymidine either in the presence of 10% of BFS (control = 113,838 +/- 6978; EGF = 119,434 +/- 9441; NS) or in its absence (control = 46,197 +/- 3335; EGF = 44,472 +/- 3493; NS). The results here reported suggest that: a) EGF may affect the proliferation of cells derived from a primary human neuroblastoma; b) this is evident by the EGF-induced increase of [3H]-thymidine incorporation in SK-N-SH cells; c) it is required the presence of other growth factors, present in the FBS, for the mitogenic action to be accomplished; d) since the pure neuroblastic SH-SY5Y cell line are refractory to the EGF, the effects observed in SK-N-SH cells probably occur on the melanocytic/glial cell subpopulation.

Insulin‐like growth factor I is the key growth factor in serum that protects neuroblastoma cells from hyperosmotic‐induced apoptosis

“…FGF can increase the expression of p75NTR in CHP100 human neuroblastoma cells as well (Taiji et al, 1992), which as mentioned previously, could actually promote apoptosis. EGF can enhance [3H]-thymidine uptake in SK-N-SH, but not SH-SY5Y cells, and only in the presence of fetal bovine serum, suggesting the need for other serum factors to produce a proliferative response (da Motta et al, 1997). Collectively, these reports coupled with the findings from the current study, indicate that while many growth factors play a role in growth and differentiation of SH-SY5Y cells, IGF-I provides the most potent protection against apoptosis.…”

Modulation of extracellular signal‐regulated kinase (ERK) activity by acute and chronic opioid treatment in neuronal and glial cell lines

“…1997). Other effects, such as EGF‐induced [ 3 H]‐thymidine incorporation, have also been described in SK‐N‐SH but not SH‐SY5Y cells (da Motta et al . 1997).…”

“…This result is intriguing because SK‐N‐SH is the parent cell line of the SH‐SY5Y cell line used in this study. However, the SK‐N‐SH cell line is composed of at least two cellular phenotypes (neuroblastic amd melanocytic/glial cells), while SH‐SY5Y is a pure subclone of the neuroblastic phenotype (da Motta et al . 1997).…”

Cell Survival Signaling in Neuroblastoma

“…113 daMotta et al showed that EGFR ligand, EGF, treatment of SK-N-SH neuroblastoma cells resulted in cell proliferation. 114 Ho and colleagues confirmed these findings, but found that the EGF-stimulated proliferation was the result of EGFR activation of the PI3K/AKT pathway. 112 Tamura et al showed that gefitinib (Table 1), an EGFR tyrosine kinase inhibitor, induced apoptosis in neuroblastoma cells.…”