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Neuroscience Letters 214 (1996) 13-16
lml
H7, an inhibitor of protein kinase C, prevents serum-induced
phosphorylation of Raf and MAP kinase in neuroblastoma cells
Hugo Cabedo, Vicente Felipo*, Maria-Dolores Mifiana, Santiago Grisolia
lnstituto de lnvestigaciones Citolfgicas de la Fundaci6n Valenciana de lnvestigaciones BiomOdicas, Amadeo de Saboya, 4, 46010 Valencia, Spain
Received 10 June 1996; revised version received 28 June 1996; accepted 28 June 1996
Abstract
We have previously shown that 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H7), an inhibitor of protein kinase C, inhibits
proliferation of neuroblastoma cells in culture. We have now tested whether the effect of H7 is mediated by MAP kinase and Raf.
It is shown that, in Neuro 2a cells, activation of protein kinase C by addition of 4~3-phorbol-12/3-myristate-13~-acetate(PMA), leads to
phosphorylation of Raf and Mitogen-activated protein kinase (MAP kinase). PMA-induced phosphorylation of these proteins is pre-
vented by H7. When quiescent Neuro 2a were stimulated to proliferate by addition of serum, Raf and MAP kinase were rapidly
phosphorylated. Serum-induced phosphorylation of Raf and MAP kinase is prevented by H7. These results suggest that, in Neuro 2a
cells, the control of proliferation by protein kinase C could be mediated by phosphorylation (and concomitant activation) of Raf and
MAP kinase.
Keywords: Protein kinase C; MAP kinase; Raf; H7; Neuroblastoma; Cell proliferation
Protein kinase C (PKC) plays an important role in the
control of cell proliferation. The involvement of PKC in
the control of cell growth was initially suggested by the
finding that PKC constitutes the receptor for mitogenic
phorbol esters, which are potent tumour promoters[12].
We have previously shown that 1-(5-isoquinolinylsulfo-
nyl)-2-methylpiperazine (H7), a non-specific inhibitor of
PKC, prevents proliferation of neuroblastoma cells (Neuro
2a) in culture [7,13,14], of other cell lines [15,16] and of
primary cultured cells from human brain tumours [ 15]. H7
also inhibits tumour cell division in mice bearing ascitic
Ehrlich's carcinoma [8]. Moreover, PKC activity is
increased in some human tumours [9]. These facts support
the idea that PKC plays a key role in the control of cell
proliferation.
Mitogen-activated protein kinases (MAP kinases), also
described as extracellular signal-regulated kinases
(ERKs), belong to a group of protein-serine/threonine
kinases that are activated in response to various stimuli
(growth factors, neurotransmitters, etc.). It has been
reported that MAP kinases are involved in the control of
* Corresponding author. Tel.: +34 6 3698500; fax: +34 6 3601453.
cell proliferation [3,5,17]. A unique feature of this family
of protein kinases is that they require dual phosphorylation
on both tyrosine and threonine residues to become fully
active [2]. It has been shown that activation of PKC can
lead to phosphorylation and activation of MAP kinase
[1,10]. It was therefore considered of interest to test
whether the effect of H7 on Neuro 2a cell proliferation
is mediated by alterations in MAP kinase.
4/3-Phorbol-12/3-myristate-13cc-acetate (PMA) was
from Molecular Probes (Eugene, OR, USA). H7 was
from Sigma (St. Louis, MO, USA).
The clonal cell line Neuro 2a, C1300 mouse neuroblas-
toma, was obtained from the American Type Culture Col-
lection. Cells were grown at 37°C in Eagle's minimum
essential medium (MEM) supplemented with 10% foetal
bovine serum, 100 IU of penicillin per ml, and 100 mg/ml
of streptomycin.
For synchronization, the cells were seeded (400000
cells/ml) in MEM without glutamine containing 0.5% foe-
tal bovine serum and antibiotics as above; after 48 h the
cells were in Go. To stimulate cell proliferation the med-
ium was removed, the cells were washed and stimulated by
addition of complete MEM with 10% foetal bovine serum.
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