Prespecification and plasticity: shifting mechanisms of cell migration.

By Peter Friedl. Current Opinion in Cell Biology, 2004

725 citations recorded by the source corpus.

Subfields: Biomedical Engineering, Cell Biology

View Paper: https://www.semanticscholar.org/paper/4f268a85e7d51a2cb473e0b88eb92ffbfdeb7a92

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In Biomedical Engineering

In Cell Biology

Citations in the corpus

TGF-&bgr; signaling and epithelial–mesenchymal transition in cancer progression (2013, neutral): “move either individually or collectively [51,52].”
The impact of jamming on boundaries of collectively moving weak-interacting cells (2012, background): “Collective cell migration is an important characteristic of morphogenesis, wound healing and the growth of a tumor front [1, 2].”
Modeling tissue morphogenesis and cancer in 3D. (2007, positive): “…MMPs, was reported to have no effect on cell invasion in another 3D collagen gel system; instead, tumor cells switched to an ameboid type of migration analogous to that used by T cells, which does not require integrins and uses different Rho-ROCK signaling (Friedl, 2004; Wyckoff et al., 2006).”
Advances in establishment and analysis of three-dimensional tumor spheroid-based functional assays for target validation and drug evaluation (2012, background): “In contrast, KNS42 cells move slowly and collectively in a radial pattern, reflecting a more mesenchymal phenotype [45,46] (Additional files 3 and 4).”
Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic. (2009, background): “like the type of ECM, the genetic alterations and a potential drug treatment [37,38,158], pointing out the possibility that they could alternatively used as a result of an adaptation of tumour cells to facilitate metastasis.”
Mitf regulation of Dia1 controls melanoma proliferation and invasiveness. (2006, background): “2005), more akin to an amoeboid form of cell invasion than the mesenchymal elongated form of migration (Friedl 2004).”
Anoikis molecular pathways and its role in cancer progression. (2013, background): “Intriguingly cell–ECM attachments are not required for amoeboid movement and focal adhesions are not organized [68,248].”
Synthetic biomaterials as instructive extracellular microenvironments for morphogenesis in tissue engineering (2005, background): “Structural ECM features, such as fibrils and pores, are often of a size compatible with cellular processes involved in migration, which may influence the strategy by which cells migrate through ECM”
Engineering microscale topographies to control the cell–substrate interface (2012, background): “Contact guidance is known to affect cellular behaviors such as adhesion, morphology, migration, and differentiation [12-16].”
Complex networks orchestrate epithelial–mesenchymal transitions (2006, background): “Indeed, there is plasticity in the way that mesenchymal cells migrate — they might migrate together as chains, or as individual cells that exhibit either cyclic extension–adhesion–retraction translocation or amoeboid-type crawlin”
Cancer invasion and the microenvironment: plasticity and reciprocity. (2011, neutral): “, and Friedl, P. (2012). Cancer invasion and resistance - interconnected processes of disease progression and therapy failure.”
Cell motility through plasma membrane blebbing (2008, background): “Consistent with this, some cancer cells preferentially use the bleb-associated amoeboid mode of invasion to bypass the requirement for extracellular matrix proteolysis or simply to switch modes of motility as an escape mechanism ( Sahai and Marshall, 2003; Friedl, 2004 ).”
The role of disturbed pH dynamics and the Na+/H+ exchanger in metastasis (2005, background): “Conditions that increase invasive capacity often provoke a dramatic shift in cell morphology from AMOEBOID MORPHOTYPE to MESENCHYMAL MORPHOTYPE , which corresponds with the increase in invasive capacit”
The role of focal-adhesion kinase in cancer — a new therapeutic opportunity (2005, background): “By contrast, amoeboid-like invasion might be independent of this FAK function, as this mode of invasion through a 3D matrix is less dependent on integrin-mediated adhesions within the matri”