Collective cell migration of thyroid carcinoma cells: a beneficial ability to override unfavourable substrates

Lobastova, Liudmila; Kraus, Dominik; Glassmann, Alexander; Khan, Dilaware; Steinhäuser, Christian; Wolff, Christina R.; Veit, Nadine; Winter, Jochen; Probstmeier, Rainer

doi:10.1007/s13402-016-0305-5

Cited by 13 publications

(8 citation statements)

References 32 publications

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“…150 μ L of methanol was added per well, and the optical density at 540 nm was measured. The LDH assay was carried out as described previously with the “LDH Cytotoxicity Assay Kit” from Roche [ 19 ].…”

Section: Methodsmentioning

confidence: 99%

Staurosporine Induces the Generation of Polyploid Giant Cancer Cells in Non-Small-Cell Lung Carcinoma A549 Cells

Glassmann¹,

Garcia

Janzen

et al. 2018

Analytical Cellular Pathology

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Cultivation of A549 non-small-cell lung carcinoma (NSCLC) cells in the presence of staurosporine (SSP) leads to a reduction or a lack of proliferation in a concentration-dependent manner. This inhibition of proliferation is accompanied by the generation of polyploid giant cancer cells (PGCCs) that are characterized by cell flattening, increased cell size, polyploidy, and polynucleation as determined by crystal violet staining, BrdU and DiI labelling, and flow cytometry as well as video time-lapse analysis. Continuous SSP treatment of A549 cells can preserve PGCCs for at least two months in a resting state. Upon removal of SSP, A549 PGCCs restart to divide and exhibit a proliferation pattern and cellular morphology indistinguishable from cells where PGCCs originally derived from. Thus, SSP-treated A549 cells represent a simple and reliable experimental model for the reversible generation of PGCCs and their subsequent experimental analysis.

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Section: Methodsmentioning

confidence: 99%

Staurosporine Induces the Generation of Polyploid Giant Cancer Cells in Non-Small-Cell Lung Carcinoma A549 Cells

Glassmann¹,

Garcia

Janzen

et al. 2018

Analytical Cellular Pathology

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“…Collective invasion is characterized by maintenance of cell-to-cell adhesion and front-rear polarity within the migrating cell unit by multicellular coordination and generation of traction force for forward migration and by remodeling of ECM. The plasticity of collectively migrating tumor cells ranges from coordinated sheets, strands, and tubes to clusters [ 65 – 68 ]. Nevertheless, tip cells or leader cells, respectively, feature mesenchymal morphology, whereas subsequent cells are structured by epithelial cell-to-cell contacts.…”

Section: Introductionmentioning

confidence: 99%

Breast Carcinoma: From Initial Tumor Cell Detachment to Settlement at Secondary Sites

Melzer

Ohe

Hass

2017

BioMed Research International

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Metastasis represents a multistep cascade of cancer cell alterations accompanied by structural and functional changes within the tumor microenvironment which may involve the induction of a retrodifferentiation program. Major steps in metastatic developments include (A) cell detachment from the primary tumor site involving epithelial-mesenchymal transition (EMT), (B) migration and invasion into surrounding tissue, (C) transendothelial intravasation into the vasculature of blood and/or lymphatic vessels as circulating tumor cells (CTCs), (D) dissemination to distant organs, and (E) extravasation of CTCs to secondary sites as disseminated tumor cells (DTCs). This article highlights some aspects of the metastatic cascade with a focus on breast cancer cells. Metastatic steps critically depend on the capability of cancer cells to adapt to distant tissues and the corresponding new microenvironment. As a consequence, increasing plasticity and developmental changes paralleled by acquisition of new cancer cell functionalities challenge a successful therapeutic approach.

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“…Cells were seeded into pre-coated (20 µg/ml galectin-3 or EHS laminin) 24-well plates (2,000 cells per well) and allowed to adhere overnight. Video time lapse analyses were then carried out as previously described (21). Briefly, the culture plates were transferred to a pre-heated (37˚C), gassed (5% CO 2 /air) and humidified chamber fitted onto an inverted microscope (Axiovert 200 M; Carl Zeiss AG) equipped with a motorized cross-stage.…”

Section: Cell Adhesion Assaymentioning

confidence: 99%

“…Galectin-3 does not promote the migration of thyroid carcinoma cells. Thyroid carcinoma cells were seeded onto plastic, galectin-3 or laminin substrata and the migration paths of individual cells were recorded for 24 h as previously described (21). Cells were mobile on a laminin substrate to varying degrees: 5.4 µm/h for B-CPAP, 20.4 µm/h for Cal-62 and 13.8 µm/h for FTC-133 cells (Fig.…”

Section: Galectin-3 From Thyroid Carcinoma Cells Harbors a Functionally Active Crdmentioning

confidence: 99%

Galectin‑3 promotes the adhesion, but not the migration of thyroid carcinoma cells in a β‑galactoside‑specific manner

Winter

Glassmann²,

Kraus

et al. 2021

World Acad Sci J

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In thyroid carcinoma cells, the soluble β-galactosidespecific lectin, galectin-3, is extra-and intracellularly expressed and plays a significant role in thyroid cancer diagnosis. The functional relevance of this molecule, particularly in its extracellular environment however, warrants further elucidation. To gain insight into this topic, the present study characterized principal functional properties of galectin-3 in 3 commonly used thyroid carcinoma cell lines (B-CPAP, Cal-62 and FTC-133) that express the molecule intra-and extracellulary. Cell-intrinsic galectin-3 harbors a functional carbohydrate recognition domain as determined by affinity purification. Moreover, cell surface expressed galectin-3 can be partially removed by treatment with lactose or asialofetuin, but not with sucrose. Thyroid carcinoma cells adhere to substrate-bound galectin-3 in a β-galactoside-specific manner, whereby only cell adhesion, but not cell migration is promoted. Thus, thyroid tumor cells harbor functional active galectin-3 that, inter alia, specifically interacts with cell surface-expressed molecular ligands in a β-galactoside-dependent manner, whereby the molecule can at least interfere with cell adhesion. The modulation of galectin-3 expression level or its ligands in such tumor cells could be of therapeutic interest and needs further experimental clarification.

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Collective cell migration of thyroid carcinoma cells: a beneficial ability to override unfavourable substrates

Abstract: Our data indicate that collective migration enables tumor cells to cross otherwise unfavourable substrate areas. This capacity seems to be independent of intercellular communication via gap junctions, whereas Rac1-dependent intracellular signalling seems to be essential.

Cited by 13 publications

References 32 publications

Staurosporine Induces the Generation of Polyploid Giant Cancer Cells in Non-Small-Cell Lung Carcinoma A549 Cells

Staurosporine Induces the Generation of Polyploid Giant Cancer Cells in Non-Small-Cell Lung Carcinoma A549 Cells

Breast Carcinoma: From Initial Tumor Cell Detachment to Settlement at Secondary Sites

Galectin‑3 promotes the adhesion, but not the migration of thyroid carcinoma cells in a β‑galactoside‑specific manner

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