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Vol. 273, Issue 4, C1290-C1297, October 1997
Department of Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294
We recently
demonstrated expression of a novel, glioma-specific
Cl
current in glial-derived
tumor cells (gliomas), including stable cell lines such as STTG1,
derived from a human anaplastic astrocytoma. We used STTG1 cells to
study whether glioma Cl
channel (GCC) activity is regulated during cell cycle progression. Cells were arrested in defined stages of cell cycle
(G0,
G1,
G1/S, S, and M phases) using serum
starvation, mevastatin, hydroxyurea, demecolcine, and cytosine
-D-arabinofuranoside. Cell
cycle arrest was confirmed by measuring
[3H]thymidine
incorporation and by DNA flow cytometry. Using whole cell patch-clamp
recordings, we demonstrate differential changes in GCC activity after
cell proliferation and cell cycle progression was selectively altered;
specifically, channel expression was low in serum-starved,
G0-arrested cells, increased
significantly in early G1,
decreased during S phase, and increased after arrest in M phase.
Although the link between the cell cycle and GCC activity is not yet
clear, we speculate that GCCs are linked to the cytoskeleton and that
cytoskeletal rearrangements associated with cell division lead to the
observed changes in channel activity. Consistent with this hypothesis,
we demonstrate the activation of GCC by disruption of F-actin using
cytochalasin D or osmotic cell swelling.
ion channels; flow cytometry; proliferation; chlorotoxin; glioblastoma; astrocytoma
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