Illuminating breast cancer invasion: diverse roles for cell–cell interactions

Cheung, Kevin; Ewald, Andrew J.

doi:10.1016/j.ceb.2014.07.003

Cited by 102 publications

(124 citation statements)

References 143 publications

(148 reference statements)

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“…The leading front of the tube, which drives collective mobility, undergoes a loosening (but not ablation) of cell junction stability, for example, by maintaining a partial EMT in which E-cadherin-based junctions gain flexibility and increase their turnover; concurrently cells in the rear position, which form the extending tube, retain stable cell -cell junctions and apicobasal polarity, and gradually downscale their migration ability (Shamir and Ewald 2015). Likely, similar reprogramming of leader cells toward loosened junction organization is active during neoplastic invasion of breast cancer cells (Cheung et al 2013;Cheung and Ewald 2014). Thus, tuning cell -cell junction stability regulates the degree of collective dynamics.…”

Section: Tissue Morphogenesis and Regenerationmentioning

confidence: 95%

Tuning Collective Cell Migration by Cell–Cell Junction Regulation

Friedl

Mayor

2017

Cold Spring Harb Perspect Biol

307

253

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Collective cell migration critically depends on cell -cell interactions coupled to a dynamic actin cytoskeleton. Important cell-cell adhesion receptor systems implicated in controlling collective movements include cadherins, immunoglobulin superfamily members (L1CAM, NCAM, ALCAM), Ephrin/Eph receptors, Slit/Robo, connexins and integrins, and an adaptive array of intracellular adapter and signaling proteins. Depending on molecular composition and signaling context, cell -cell junctions adapt their shape and stability, and this gradual junction plasticity enables different types of collective cell movements such as epithelial sheet and cluster migration, branching morphogenesis and sprouting, collective network migration, as well as coordinated individual-cell migration and streaming. Thereby, plasticity of cell -cell junction composition and turnover defines the type of collective movements in epithelial, mesenchymal, neuronal, and immune cells, and defines migration coordination, anchorage, and cell dissociation. We here review cell -cell adhesion systems and their functions in different types of collective cell migration as key regulators of collective plasticity.

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Section: Tissue Morphogenesis and Regenerationmentioning

confidence: 95%

Tuning Collective Cell Migration by Cell–Cell Junction Regulation

Friedl

Mayor

2017

Cold Spring Harb Perspect Biol

307

253

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“…Cells grown on 2D culture surfaces display abnormal cell-cell interactions (17), cell-matrix interactions (if present; ref. 18) and are prone to spatial artifacts such as apicalbasal polarization of fibroblasts (19) or inappropriate polarity and differentiation of epithelial cells (20).…”

Section: Introductionmentioning

confidence: 99%

3-Dimensional Patient-Derived Lung Cancer Assays Reveal Resistance to Standards-of-Care Promoted by Stromal Cells but Sensitivity to Histone Deacetylase Inhibitors

Onion

Argent

Reece-Smith

et al. 2016

Molecular Cancer Therapeutics

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There is a growing recognition that current preclinical models do not reflect the tumor microenvironment in cellular, biological, and biophysical content and this may have a profound effect on drug efficacy testing, especially in the era of molecular-targeted agents. Here, we describe a method to directly embed low-passage patient tumor-derived tissue into basement membrane extract, ensuring a low proportion of cell death to anoikis and growth complementation by coculture with patient-derived cancer-associated fibroblasts (CAF). A range of solid tumors proved amenable to growth and pharmacologic testing in this 3D assay. A study of 30 early-stage non-small cell lung cancer (NSCLC) specimens revealed high levels of de novo resistance to a large range of standard-of-care agents, while histone deacetylase (HDAC) inhibitors and their combination with antineoplastic drugs displayed high levels of efficacy. Increased resistance was seen in the presence of patient-derived CAFs for many agents, highlighting the utility of the assay for tumor microenvironment-educated drug testing. Standard-of-care agents showed similar responses in the 3D ex vivo and patient-matched in vivo models validating the 3D-Tumor Growth Assay (3D-TGA) as a high-throughput screen for close-to-patient tumors using significantly reduced animal numbers. Mol Cancer Ther; 15(4); 753-63. Ó2016 AACR.

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“…cadherin | wound healing | biomaterial | biomimetic | collective migration T issue-tissue interfaces play important roles in a variety of cellular processes from morphogenesis (1,2) to wound healing or self-healing (3,4) and to tumorigenesis (5,6). During selfhealing, two separated tissues of the same type meet and merge to heal an injury (3,7,8).…”

mentioning

confidence: 99%

“…Abercrombie and Heaysman (8) first hypothesized that cell-cell adhesion served a dual role in inhibiting migratory polarity and promoting cell-cell recognition and attachment between homotypic (mutually similar) cells and tissues (4)(5)(6)11). Homotypic adhesive interactions often involve cadherins.…”

mentioning

confidence: 99%

Epithelial self-healing is recapitulated by a 3D biomimetic E-cadherin junction

Cohen

Gloerich

Nelson

2016

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

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Epithelial monolayers undergo self-healing when wounded. During healing, cells collectively migrate into the wound site, and the converging tissue fronts collide and form a stable interface. To heal, migrating tissues must form cell-cell adhesions and reorganize from the front-rear polarity characteristic of cell migration to the apicalbasal polarity of an epithelium. However, identifying the "stop signal" that induces colliding tissues to cease migrating and heal remains an open question. Epithelial cells form integrin-based adhesions to the basal extracellular matrix (ECM) and E-cadherinmediated cell-cell adhesions on the orthogonal, lateral surfaces between cells. Current biological tools have been unable to probe this multicellular 3D interface to determine the stop signal. We addressed this problem by developing a unique biointerface that mimicked the 3D organization of epithelial cell adhesions. This "minimal tissue mimic" (MTM) comprised a basal ECM substrate and a vertical surface coated with purified extracellular domain of E-cadherin, and was designed for collision with the healing edge of an epithelial monolayer. Three-dimensional imaging showed that adhesions formed between cells, and the E-cadherin-coated MTM resembled the morphology and dynamics of native epithelial cell-cell junctions and induced the same polarity transition that occurs during epithelial self-healing. These results indicate that E-cadherin presented in the proper 3D context constitutes a minimum essential stop signal to induce self-healing. That the Ecad:Fc MTM stably integrated into an epithelial tissue and reduced migration at the interface suggests that this biointerface is a complimentary approach to existing tissue-material interfaces.cadherin | wound healing | biomaterial | biomimetic | collective migration

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Illuminating breast cancer invasion: diverse roles for cell–cell interactions

Cited by 102 publications

References 143 publications

Tuning Collective Cell Migration by Cell–Cell Junction Regulation

Tuning Collective Cell Migration by Cell–Cell Junction Regulation

3-Dimensional Patient-Derived Lung Cancer Assays Reveal Resistance to Standards-of-Care Promoted by Stromal Cells but Sensitivity to Histone Deacetylase Inhibitors

Epithelial self-healing is recapitulated by a 3D biomimetic E-cadherin junction

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