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Trifluoperazine inhibits spreading and migration of cells in culture
Author(s) -
Connor Charles G.,
Brady Richard C.,
Brownstein Barbara L.
Publication year - 1981
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041080303
Subject(s) - trifluoperazine , microbiology and biotechnology , chemistry , biology , biochemistry , calmodulin , enzyme
Trifluoperazine (TFP) blocks spreading and migration of cultured mammalian cells. These are calcium‐dependent and microfilament‐mediated processes. Calmodulin, a regulator of many calcium‐dependent processes in cells, is selectively inhibited by TFP. Cell spreading on a plastic‐ or collagen‐coated substratum was reversibly inhibited by 10 μM TFP. The drug blocks cell spreading even in the presence of 1 mM cAMP. TFP is as effective as cytochalasin B (CB), an inhibitor of microfilament function, in blocking cell spreading. All cell lines tested, whether “normal” or virally transformed, failed to spread in TFP. The drug, at a concentration sufficient to inhibit spreading, does not interfere with the initial attachment of a cell to a plastic surface. Cells plated in the presence of 10 μM TFP attach at a rate and to an extent equal to untreated controls. TFP added to already spread cells results in a reversible cell rounding. Detection of fibronectin by indirect immunofluorescence suggests TFP‐induced cell rounding is not due to shedding of fibronectin from the cell surface. TFP reversibly blocks cell migration into a wound edge almost as effectively as CB. We suggest that TFP interferes with these microfilament‐mediated functions by direct action on the microfilaments or indirect action by inactivating calmodulin.