The role of cancer cell motility in invasion

Sträuli, Peter; Haemmerli, Gisela

doi:10.1007/bf00047660

Cited by 71 publications

(46 citation statements)

References 99 publications

(78 reference statements)

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“…To determine whether this Fourier method for (19)(20)(21)(22)(23)(24)(25). Cell motility may have an essential role in metastasis (16,20,22,23,25).…”

Section: Resultsmentioning

confidence: 99%

Fourier analysis of cell motility: correlation of motility with metastatic potential.

Partin

Schoeniger

Mohler

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

170

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We report the development of a computerized, mathematical system for quantitating the various types of cell motility. This Fourier analysis method simultaneously quantifies for individual cells (i) temporal changes in cell shape represented by cell ruffling, undulation, and pseudopodal extension, (ii) cell translation, and (iii) average cell size and shape. This spatial-temporal Fourier analysis was tested on a series of well-characterized animal tumor cell lines of rat prostatic cancer to study in a quantitative manner the corre- RESULTS AND DISCUSSIONCell Culture, Microscopy, and Image Analysis. Fig. 1

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“…To determine whether this Fourier method for (19)(20)(21)(22)(23)(24)(25). Cell motility may have an essential role in metastasis (16,20,22,23,25).…”

Section: Resultsmentioning

confidence: 99%

Fourier analysis of cell motility: correlation of motility with metastatic potential.

Partin

Schoeniger

Mohler

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

170

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“…However, the results from experiments on intercellular aggregation, disaggregation and adhesion also indicate that this restriction on movement is not due to a simple increase in intercellular adhesiveness of tight cells. It has long been thought possible that highly motile tumour cells might more easily invade surrounding host tissue (Willis, 1934), although it has also been suggested that locomotion is not essential for invasion (Strauli & Haemmerli, 1984). Studies in vitro have revealed conflicting results (Hart, 1979;Varani & Lovett, 1982;Volk et al, 1984).…”

Section: Aggregation and Disaggregation The Results Inmentioning

confidence: 99%

Morphological and metastatic murine melanoma variants: motility, adhesiveness, cell surface and in vivo properties

Clark¹,

Js²,

Sidebottom³

1987

Br J Cancer

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The results show enhanced differences in metastatic potential of tight and loose clones after selective cloning and that there may be important differences in motility and cell-substrate interactions. Foulds (1949) introduced the term tumour progression to describe the process by which some tumours become more malignant during their growth. Nowell (1976) attributed this to genetic instability, although genetic or epigenetic processes could result in the emergence of variant cells with growth advantages which differ from the main population in the expression of specific characters (Frost & Kerbel, 1983;Schimke et al., 1985).The existence within tumours of cells heterogeneous for the expression of a wide range of in vivo and in vitro characters is well documented (for reviews see Heppner, 1984;Nicolson, 1984).We have previously reported heterogeneity of clonal morphology in a metastatic melanomaxlymphocyte hybrid tumour cell line (Clark & Sidebottom, 1984). These variants grow either as tight or loose colonies and the isolation of cell lines, stable for clonal morphology, which have low or high metastatic phenotypes has been described (Clark & Sidebottom, 1984). The morphology and patterns of growth of these variants suggests a number of ways in which these cells may differ and which might account for their behavioural differences in vitro. These include intercellular and cell-substrate adhesion and motility, which in turn are dependent upon cell surface properties. Various stages of the metastatic cascade, for example local invasion or tumourcapillary endothelium adhesion are partially dependent upon intercellular and cell-substrate adhesion and motility (Weiss, 1980;Varani et al., 1980;Nicolson et al., 1986). The cell surface has an important role in these interactions and has been extensively studied for correlations with metastasis and organ colonization (Turner, 1982;Nicolson, 1984).Observation and measurement of adhesion and motility in vivo have inherent difficulties, but these characters can be investigated in vitro and some clues about their possible significance in vivo thereby gained (Briles & Kornfeld, 1978; Hart, 1979;Vollmers & Birchmeier, 1983;McCarthy et al., 1985).We have, therefore, looked at the adhesive and motile properties of tight and loose cells and also examined their cell surfaces by lectin binding to PAGE separated glycoproteins, radio-iodination of proteins and quantitation of sialic acid content. (Sidebottom & Clark, 1983). The cell lines 1G8(6F) and 1G3(4E) were selected from F87.CI.6T2 cells for tight or loose clonal morphology respectively and their in vitro and in vivo properties have been described elsewhere (Clark & Sidebottom, 1984). Cells were maintained in MEM +10% newborn calf serum (Flow) (cMEM) and subcultured when confluent; they were regularly tested for mycoplasma and found to be negative. Wiscm cells were derived from explanted hearts from one day old Wistar rats and were maintained in DMEM + 10% foetal calf serum (Gibco) +10% tryptose phosphate broth (Difco). To prod...

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“…E-Cadherin (CDH1) is mainly expressed in epithelial cells. Reduced CDH1 expression is associated with dysfunction of cell-cell adhesion system and has been shown to promote tumor invasion and metastasis (Strauli & Haemmerli 1984, Volk et al 1984. Decreased expression of CDH1 correlates with high histological grade and aggressive behavior and has been reported in 10-20% of type I and in 80-90% of type II human endometrial tumors (reviewed in Lax (2004Lax ( , 2007 and Liu (2007)).…”

Section: E Samuelson Et Al: Molecular Classification Of Bdii Rat Eacmentioning

confidence: 99%

Molecular classification of spontaneous endometrial adenocarcinomas in BDII rats

Samuelson

Hedberg²,

Nilsson³

et al. 2009

Endocrine-Related Cancer

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Female rats of the BDII/Han inbred strain are prone to spontaneously develop endometrial carcinomas (EC) that in cell biology and pathogenesis are very similar to those of human. Human EC are classified into two major groups: Type I displays endometroid histology, is hormone-dependent, and characterized by frequent microsatellite instability and PTEN, K-RAS, and CTNNB1 (b-Catenin) mutations; Type II shows non-endometrioid histology, is hormone-unrelated, displays recurrent TP53 mutation, CDKN2A (P16) inactivation, over-expression of ERBB2 (Her2/neu), and reduced CDH1 (Cadherin 1 or E-Cadherin) expression. However, many human EC have overlapping clinical, morphologic, immunohistochemical, and molecular features of types I and II. The EC developed in BDII rats can be related to type I tumors, since they are hormone-related and histologically from endometrioid type. Here, we combined gene sequencing (Pten, Ifr1, and Ctnnb1) and real-time gene expression analysis (Pten, Cdh1, P16, Erbb2, Ctnnb1, Tp53, and Irf1) to further characterize molecular alterations in this tumor model with respect to different subtypes of EC in humans. No mutation in Pten and Ctnnb1 was detected, whereas three tumors displayed sequence aberrations of the Irf1 gene. Significant down regulation of Pten, Cdh1, p16, Erbb2, and Ctnnb1 gene products was found in the tumors. In conclusion, our data suggest that molecular features of spontaneous EC in BDII rats can be related to higher-grade human type I tumors and thus, this model represents an excellent experimental tool for research on this malignancy in human.

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The role of cancer cell motility in invasion

Cited by 71 publications

References 99 publications

Fourier analysis of cell motility: correlation of motility with metastatic potential.

Fourier analysis of cell motility: correlation of motility with metastatic potential.

Morphological and metastatic murine melanoma variants: motility, adhesiveness, cell surface and in vivo properties

Molecular classification of spontaneous endometrial adenocarcinomas in BDII rats

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