The BE (2)-M17 neuroblastoma cell line synthesizes and secretes corticotropin-releasing factor

1994 ◽  
Vol 654 (1) ◽  
pp. 159-162 ◽  
Author(s):  
John W. Kasckow ◽  
David G. Parkes ◽  
Michael J. Owens ◽  
Mark D. Stipetic ◽  
Jin-Hee Han ◽  
...  
Keyword(s):  
Cell Line ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cell Line ◽  
Corticotropin Releasing Factor

NOTEExpression of prolactin receptors and regulation of cell proliferation by prolactin, corticotropin-releasing factor, and corticosterone in a neuroblastoma cell line

2002 ◽  
Vol 80 (4) ◽  
pp. 475-482 ◽  
Author(s):  
Y N Mohammad ◽  
M Perone ◽  
L Wang ◽  
P M Ingleton ◽  
M G Castro ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Line ◽  
Neuroblastoma Cell ◽  
Fold Increase ◽  
Neuroblastoma Cell Line ◽  
Corticotropin Releasing Factor ◽  
Stress Axis ◽  
Prolactin Receptors ◽  
Neuro2a Cell ◽  
Neuro2a Cells

The aetiology of neuroblastoma remains obscure, although a number of neuropeptides have been implicated in its pathogenesis. Using the mouse neuroblastoma cell line Neuro2a as a model, we have investigated the mitogenic actions of prolactin (PRL) and two hypothalamo–pituitary–adrenal stress axis hormones, corticotropin-releasing factor (CRF) and corticosterone. Using established polyclonal PRL receptor antisera with immunofluorescence cytochemistry, we show that the Neuro2a cells possess immunoreactive forms of both the long and short forms of the receptor. PRL and CRF were effective as mitogens in Neuro2a cell cultures, where a 10–7 M concentration of PRL or CRF elicited a two-fold increase in the numbers of cells after 72 h (p < 0.0001). Corticosterone, however, attenuated their proliferation. These data suggest that prolactin may act to increase the proliferation and regulation of neuroblastomas and that the effects of PRL may be modified by hypothalamo–pituitary–adrenal hormones.Key words: cell proliferation, mitogens, neuroblasts, stress, cancer.

scholarly journals Pyrido[2′,1′:2,3]imidazo[4,5-c]isoquinolin-5-amines as Potential Cytotoxic Agents against Human Neuroblastoma

2021 ◽  
Vol 14 (8) ◽  
pp. 750
Author(s):  
Zahira Tber ◽  
Mohammed Loubidi ◽  
Jabrane Jouha ◽  
Ismail Hdoufane ◽  
Mümin Alper Erdogan ◽  
...  
Keyword(s):  
Cell Line ◽  
Drug Exposure ◽  
Caspase 3 ◽  
Biological Activities ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cell Line ◽  
Cytotoxic Agents ◽  
Human Neuroblastoma Cell ◽  
Human Neuroblastoma ◽  
Parp 1

We report herein the evaluation of various pyrido[2′,1′:2,3]imidazo[4,5-c]isoquinolin-5-amines as potential cytotoxic agents. These molecules were obtained by developing the multicomponent Groebke–Blackburn–Bienaymé reaction to yield various pyrido[2′,1′:2,3]imidazo[4,5-c]quinolines which are isosteres of ellipticine whose biological activities are well established. To evaluate the anticancer potential of these pyrido[2′,1′:2,3]imidazo[4,5-c]isoquinolin-5-amine derivatives in the human neuroblastoma cell line, the cytotoxicity was examined using the WST-1 assay after 72 h drug exposure. A clonogenic assay was used to assess the ability of treated cells to proliferate and form colonies. Protein expressions (Bax, bcl-2, cleaved caspase-3, cleaved PARP-1) were analyzed using Western blotting. The colony number decrease in cells was 50.54%, 37.88% and 27.12% following exposure to compounds 2d, 2g and 4b respectively at 10 μM. We also show that treating the neuroblastoma cell line with these compounds resulted in a significant alteration in caspase-3 and PARP-1 cleavage.

scholarly journals Divergent Pathways Regulate Ligand-Independent Activation of ERα in SK-N-BE Neuroblastoma and COS-1 Renal Carcinoma Cells

1998 ◽  
Vol 12 (6) ◽  
pp. 835-841
Author(s):  
Cesare Patrone ◽  
Elisabetta Gianazza ◽  
Sabrina Santagati ◽  
Paola Agrati ◽  
Adriana Maggi
Keyword(s):  
Cell Line ◽  
Intracellular Signaling ◽  
Steroid Receptors ◽  
Neuroblastoma Cell ◽  
Cross Coupling ◽  
Activation Function ◽  
Neuroblastoma Cell Line ◽  
Membrane Receptors ◽  
Insulin Dependent ◽  
The Cross

Abstract The α-estrogen receptor (ERα) transcriptional activity can be regulated either by binding to the cognate ligand or by intracellular signaling pathways responsive to a variety of factors acting through cell membrane receptors. Studies carried out in HeLa and COS-1 cells demonstrated that the cross-coupling between estrogen and growth factor receptors is mediated by p21ras and requires phosphorylation of a specific serine residue (Ser 118 in the human ERα and Ser 122 in mouse ERα) located in the ERα N-terminal activation function 1 (AF-1). Likewise, in the SK-N-BE neuroblastoma cell line p21ras is involved in the cross-coupling between insulin and ERα receptors. However, in this cell line Ser 122 is not necessary for insulin-dependent activation of unliganded ERα. In addition, after insulin activation, the electrophoretic mobility associated to serine hyperphosphorylation of ERα in SK-N-BE and in COS-1 cells is different. Our study rules out the possibility of tyrosine phosporylation in unliganded ERα activation by means of transactivation studies of ERα tyrosine mutants and analysis of Tyr phosphorylation immunoreactivity. The two cofactors for steroid receptors RIP 140 and SRC-1 do not seem to be specifically involved in the insulin-induced ERα transactivation. The present study demonstrates the possibility of an alternative, cell-specific pathway of cross-coupling between intracellular and membrane receptors, which might be of importance for the understanding of the physiological significance of this mode of activation in the nervous system.

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