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Okadaic acid co‐induces vimentin expression and cell cycle arrest in MPC‐11 mouse plasmacytoma cells
Author(s) -
Giese G.,
Wiegers W.,
Kubbies M.,
Scherbarth A.,
Traub P.
Publication year - 1995
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.1041630117
Subject(s) - okadaic acid , vimentin , phosphatase , cell cycle , microbiology and biotechnology , cell cycle checkpoint , chemistry , plasmacytoma , biology , cell , biochemistry , phosphorylation , immunology , multiple myeloma , immunohistochemistry
The effect of the tumor promoter okadaic acid on cell cycle progression and on vimentin expression in MPC‐11 mouse plasmacytoma cells was compared with that of the tumor promoter 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA). Cell cycle progression of asynchronously grown MPC‐11 cells was inhibited by both agents, but, in contrast to the G1 phase arrest caused by TPA, okadaic acid gave rise to G2/M phase and S phase arrest. This effect of okadaic acid was delayed significantly compared to the TPA‐caused arrest. Furthermore, okadaic acid was able to induce vimentin expression to an extent comparable to the TPA response. However, vimentin expression was markedly delayed in okadaic acid‐treated relative to TPA‐treated cells. Another protein phosphatase inhibitor, calyculin A, also induced cell cycle changes and vimentin expression at concentrations at or above 1 × 10 −9 M. Based on these observations, we suggest an involvement of protein phosphatase 1 (possibly also phosphatase 2A and/or other phosphatases) in both the G2/M cell cycle block and the induction of vimentin expression in MPC‐11 cells by okadaic acid. © 1995 Wiley‐Liss, Inc.