COMPARATIVE RESEARCH OF NORMAL AND TRANSFORMED FIBROBLAST SPREADING. THE ROLE OF MICROFILAMENT POLYMERIZATION AND
ACTIN-MYOSIN CONTRACTILITY
M. S. Shutova, A. Y. Alexandrova
Institute of Carcinogenesis, N. N. Blokhin Cancer Research Center RAMS, Moscow;
e-mail: tonya_alex@yahoo.com
Polymerization of microfilaments and their subsequent rearrangements under control of actin-myosin interactions are two main processes underlined morphogenetic
reactions of cells. We studied their role during spreading of normal and transformed REF52tetRas fibroblasts with adjustable ras oncogene expression. Treatment
with inhibitors of cell contractility (Y27532 or blebbistatin) led to disappearance of actin bundles and focal adhesions, but both normal and transformed cells preserved high
pseudopodial activity. Spreading was considerably accelerated in normal cells and less accelerated in ras-transformed cells under these conditions. When actin
polymerization was suppressed with low concentrations of latrunculin A, stress-fibrills and focal contacts were preserved, but lamellipodial activity was lost in normal cells,
so spreading was dramatically inhibited. In the case of transformed fibroblasts, actin bundles and focal adhesions virtually disappeared, but pseudopofial activity was not lost
and spreading was suppressed to a lesser extent. Therefore, the most essential process in regulation of cell spreading and polarization is microfilament polymerization at
the leading edge. Incidentally, ras-transformed cells are less sensitive to inhibitors affecting cytoskeletal stracture than non-transfonned ones. Possible mechanisms
underlying these diversities are discussed.
Key words: lamellipodium, stress fibers, Rho-kinase, cell area, extension
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