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.

Abstract 1683: ALK F1174L kinase activity as driver of cell proliferation in neuroblastoma cell line models and neuroblastoma tumors

2012 ◽  
Author(s):  
Riet Hilhorst ◽  
Liesbeth Hovestad ◽  
Rik de Wijn ◽  
Dirk Pijnenburg ◽  
Rob Ruijtenbeek ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Line ◽  
Kinase Activity ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cell Line

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

scholarly journals Propranolol Inhibits the Proliferation of Human Glioblastoma Cell Lines Through Notch1 and Hes1 Signaling System

2021 ◽  
Author(s):  
Hyun Sik Kim ◽  
Young Han Park ◽  
Mi Jung Kwon ◽  
Joon Ho Song ◽  
In Bok Chang
Keyword(s):  
Cell Proliferation ◽  
Cell Line ◽  
Cell Lines ◽  
Mtt Assay ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cell Line ◽  
Glioblastoma Cell ◽  
Rt Pcr ◽  
Human Glioblastoma ◽  
Glioblastoma Cell Lines

Abstract PurposeThe anti-tumor effect of the beta-adrenergic receptor antagonist propranolol in breast cancer is well known; however, its activity in glioblastoma is not well-evaluated. The Notch-Hes pathway is known to regulate cell differentiation, proliferation, and apoptosis. We investigated the effect of propranolol to human glioblastoma cell lines, and the role of Notch and Hes signaling in this process.MethodsWe performed immunohistochemical staining on 31 surgically resected primary human glioblastoma tissues. We also used glioblastoma cell lines of U87-MG, LN229, and neuroblastoma cell line of SH-SY5Y in this study. The effect of propranolol and isoproterenol on cell proliferation was evaluated using the MTT assay (absorbance 570nm). The impact of propranolol on gene expression (Notch and Hes) was evaluated using real-time (RT) PCR, whereas protein levels of Notch1 and Hes1 were measured using western blotting (WB), simultaneously. Small interfering RNA (siRNA) was used to suppress the Notch gene to investigate its role in the proliferation of glioblastoma.ResultsPropranolol and isoproterenol caused a dose-dependent decrease in cell proliferation (MTT assay). RT-PCR showed an increase in Notch1 and Hes1 expression by propranolol, whereas WB demonstrated increase in Notch1 protein, but a decrease in Hes1 by propranolol. The proliferation of U87-MG and LN229 was not significantly suppressed after transfection with Notch siRNA.ConclusionThese results demonstrated that propranolol suppressed the proliferation of glioblastoma cell lines and neuroblastoma cell line, and Hes1 was more closely involved than Notch1 was in glioblastoma proliferation.

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.

Sign in / Sign up

Export Citation Format

Share Document