Cell motility is inhibited by the antiepileptic compound, valproic acid and its teratogenic analogues

Walmod, Peter S.; Foley, Andrew; Berezin, Anton; Ellerbeck, Ursula; Nau, Heinz; Bock, Elisabeth; Berezin, Vladimir

doi:10.1002/(sici)1097-0169(1998)40:3<220::aid-cm2>3.0.co;2-h

Cited by 32 publications

(15 citation statements)

References 52 publications

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“…To investigate the role of RhoA in cell motility, random locomotion of single cells was evaluated by use of time-lapse video-recording and image analysis [Walmod et al, 1998. L929 fibroblast cells were transiently transfected with plasmids encoding dominant negative (N19) and constitutively activated (V14) mutants of RhoA to determine their role in cell morphology and motility.…”

Section: Resultsmentioning

confidence: 99%

“…Random cell motility was evaluated by use of time-lapse video recording and image analysis as described previously [Walmod et al, 1998. Tissue culture dishes tightly sealed with adhesive tape were placed on a thermostatically controlled stage (Lincam Scientific Instruments Ltd., Surrey, UK) mounted on a Nikon Diaphot 300 inverted microscope (Nikon, Copenhagen, Denmark).…”

Section: Video Recordingmentioning

confidence: 99%

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The role of RhoA in the regulation of cell morphology and motility

Tkach¹,

Bock²,

Berezin³

2005

Cell Motil. Cytoskeleton

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Members of the Rho family of small GTPases are key regulators of the actin cytoskeleton, particularly in relation to the cell shape changes and the adhesion dynamic that drive cell migration. Here, we report the effect of activation or inhibition of the function of RhoA on cell motility and morphology. Both in the presence and the absence of serum, expression of constitutively active RhoA dramatically inhibited L929 fibroblasts' cell motility, and induced a rounding of the cells and a decrease in the number of processes per cell. In contrast, expression of a dominant negative mutant of RhoA had no effect on cell motility or morphology in steady-state conditions with or without serum in the medium. Inhibition of p160ROCK, a kinase effector of RhoA, only partially inhibited cell migration. Conversely, when cells were submitted to a period of serum deprivation followed by addition of serum, inhibition of endogenous RhoA by expression of the dominant negative mutant of RhoA impeded cell motility after serum stimulation. Thus, RhoA activity is required for stimulation of cell locomotion by serum factors. It was also observed that the addition of serum factors to quiescent L929 and NR6wtEGFR fibroblasts resulted in a delayed motility response of several hours compared to the immediately induced morphological changes, indicating the absence of a previously assumed direct correlation between changes in cell motility and cell morphology in response to serum addition. The motility response of L929 and NR6wtEGFR fibroblasts to serum stimulation required protein synthesis. Cell Motil.

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Section: Resultsmentioning

confidence: 99%

Section: Video Recordingmentioning

confidence: 99%

The role of RhoA in the regulation of cell morphology and motility

Tkach¹,

Bock²,

Berezin³

2005

Cell Motil. Cytoskeleton

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“…At 24 h after transfection, cells were seeded at a density of 4 Â 10 3 cells/cm 2 and grown for 24 h. Random cell motility was evaluated by use of time-lapse video-recording and image analysis as described previously (Walmod et al, 1998;2000). Analysis of cell motility and morphology was performed using the image processing software PRIMA (Protein Laboratory, Copenhagen, Denmark).…”

Section: Evaluation Of Cell Motilitymentioning

confidence: 99%

Role of the Fos family members, c-Fos, Fra-1 and Fra-2, in the regulation of cell motility

Tkach¹,

Tulchinsky

Lukanidin

et al. 2003

Oncogene

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The AP-1 transcription factor is composed of members of the Fos, Jun and ATF families, and plays a key role in tumor progression. We investigated whether Fos proteins regulate cell motility, and if so, whether this capacity is related to their transactivation potential. Two cell lines with different expression profiles of AP-1 were employed focusing on the Fos-family members c-Fos, Fra-1 and Fra-2. Transactivation motifs are found in c-Fos, but not in Fra-1 or Fra-2. The adenocarcinoma CSML0 cells display a low motility and do not express Fra-1 or Fra-2, and only very little c-Fos. In contrast, the fibroblastoid L929 cells express both Fra-1 and Fra-2, but no c-Fos, and these cells display a high motility. Transfection with Fra-1 or c-Fos, but not with Fra-2, strongly enhanced the motility of CSML0 cells. The effect of Fra-1 required the presence of the N-terminal domain of this protein.Conversely, transfection with a Fos dominant-negative mutant or with anti-sense fra-1 or fra-2, strongly reduced the motility of L929 cells. Changes in cell motility correlated with the morphological appearance and the degree of contact with the substratum. We conclude that Fos proteins have distinct roles in the regulation of cell motility.

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“…The cells were grown for 48 h in Dulbecco modified Eagle medium containing 10% fetal calf serum in the presence or absence of DOX (2 g/ml). Video recording and determination of random cell motility were performed as described previously (84). Briefly, the six-well tissue culture dishes (Nunc, Roskilde, Denmark) were placed on a thermostatically controlled stage (Lincam Scientific Instruments Ltd., Surrey, England) mounted on a Diaphot 300 inverted microscope equipped with phasecontrast optics and a modified Plexiglas incubator (Nikon, Tokyo, Japan).…”

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Fra-1 Induces Morphological Transformation and Increases In Vitro Invasiveness and Motility of Epithelioid Adenocarcinoma Cells

Kustikova

Крамеров

Grigorian

et al. 1998

Molecular and Cellular Biology

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170

146

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Two cell lines originating from a common ancestral tumor, CSML0 and CSML100, were used as a model to study AP-1 transcription factors at different steps of tumor progression. CSML0 cells have an epithelial morphology; they express epithelial but not mesenchymal markers and are invasive neither in vitro nor in vivo. CSML100 possesses all characteristics of a highly progressive carcinoma. These cells do not form tight contacts, are highly invasive in vitro, and are metastatic in vivo. AP-1 activity was considerably higher in CSML100 cells than in CSML0 cells. There was a common predominant Jun component, namely, JunD, detected in both cell lines. We found that the enhanced level of AP-1 in CSML100 cells was due to high expression of Fra-1 and Fra-2 proteins, which were undetectable in CSML0 nuclear extracts. Analysis of the transcription of different AP-1 members in various cell lines derived from tumors of epithelial origin revealed a correlation of fra-1 expression with mesenchymal characteristics of carcinoma cells. Moreover, we show here for the first time that the expression of exogenous Fra-1 in epithelioid cells results in morphological changes that resemble fibroblastoid conversion. Cells acquire an elongated shape and become more motile and invasive in vitro. Morphological alterations were accompanied by transcriptional activation of certain genes whose expression is often induced at late stages of tumor progression. These data suggest a critical role of the Fra-1 protein in the development of epithelial tumors.

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Cell motility is inhibited by the antiepileptic compound, valproic acid and its teratogenic analogues

Cited by 32 publications

References 52 publications

The role of RhoA in the regulation of cell morphology and motility

The role of RhoA in the regulation of cell morphology and motility

Role of the Fos family members, c-Fos, Fra-1 and Fra-2, in the regulation of cell motility

Fra-1 Induces Morphological Transformation and Increases In Vitro Invasiveness and Motility of Epithelioid Adenocarcinoma Cells

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