Local light-activation of the Src oncoprotein in an epithelial monolayer promotes collective extrusion

[1]  A. Grichine,et al.  Molecular flux control encodes distinct cytoskeletal responses by specifying SRC signaling pathway usage , 2019, bioRxiv.

[2]  G. Salbreux,et al.  Tissue curvature and apicobasal mechanical tension imbalance instruct cancer morphogenesis , 2019, Nature.

[3]  J. Camonis,et al.  Collective stresses drive competition between monolayers of normal and Ras-transformed cells. , 2018, Soft matter.

[4]  S. De Renzis,et al.  Guided morphogenesis through optogenetic activation of Rho signalling during early Drosophila embryogenesis , 2018, Nature Communications.

[5]  E. Furth,et al.  EMT Subtype Influences Epithelial Plasticity and Mode of Cell Migration. , 2018, Developmental cell.

[6]  J. Fredberg,et al.  Long-lived force patterns and deformation waves at repulsive epithelial boundaries. , 2017, Nature materials.

[7]  Michael Z. Lin,et al.  Understanding CRY2 interactions for optical control of intracellular signaling , 2017, Nature Communications.

[8]  J. Miyazaki,et al.  Cell competition with normal epithelial cells promotes apical extrusion of transformed cells through metabolic changes , 2017, Nature Cell Biology.

[9]  Chwee Teck Lim,et al.  Topological defects in epithelia govern cell death and extrusion , 2017, Nature.

[10]  G. Charras,et al.  Optogenetic control of cellular forces and mechanotransduction , 2017, Nature Communications.

[11]  Anh Phuong Le,et al.  Epithelial Cell Packing Induces Distinct Modes of Cell Extrusions , 2016, Current Biology.

[12]  C. Bradshaw,et al.  Mechanical cell competition kills cells via induction of lethal p53 levels , 2016, Nature Communications.

[13]  Frank Jülicher,et al.  Interface Contractility between Differently Fated Cells Drives Cell Elimination and Cyst Formation , 2016, Current Biology.

[14]  Eduardo Moreno,et al.  Tissue Crowding Induces Caspase-Dependent Competition for Space , 2016, Current Biology.

[15]  M. Dahan,et al.  Predictive Spatiotemporal Manipulation of Signaling Perturbations Using Optogenetics. , 2015, Biophysical journal.

[16]  Yasuyuki Fujita,et al.  EDAC: Epithelial defence against cancer-cell competition between normal and transformed epithelial cells in mammals. , 2015, Journal of biochemistry.

[17]  Eshel Ben-Jacob,et al.  Implications of the Hybrid Epithelial/Mesenchymal Phenotype in Metastasis , 2015, Front. Oncol..

[18]  B. Cui,et al.  Optogenetic control of intracellular signaling pathways. , 2015, Trends in biotechnology.

[19]  Mfi.  Statics and Dynamics , 2014 .

[20]  G. Wayne Brodland,et al.  Forces driving epithelial wound healing , 2014, Nature Physics.

[21]  Orion D. Weiner,et al.  Illuminating cell signalling with optogenetic tools , 2014, Nature Reviews Molecular Cell Biology.

[22]  Robert W Style,et al.  Traction force microscopy in physics and biology. , 2014, Soft matter.

[23]  Hannah G. Yevick,et al.  Emergence of collective modes and tri-dimensional structures from epithelial confinement , 2014, Nature Communications.

[24]  Nicholas A. Hamilton,et al.  Cortical F-actin stabilization generates apical–lateral patterns of junctional contractility that integrate cells into epithelia , 2014, Nature Cell Biology.

[25]  P. Silberzan,et al.  Border forces and friction control epithelial closure dynamics. , 2014, Biophysical journal.

[26]  Romain Levayer,et al.  Mechanisms of cell competition: Themes and variations , 2013, The Journal of cell biology.

[27]  Pascal Silberzan,et al.  Automated velocity mapping of migrating cell populations (AVeMap) , 2012, Nature Methods.

[28]  P. De Camilli,et al.  Optogenetic control of phosphoinositide metabolism , 2012, Proceedings of the National Academy of Sciences.

[29]  Chi-Bin Chien,et al.  Crowding induces live cell extrusion to maintain homeostatic cell numbers in epithelia , 2012, Nature.

[30]  Jonathan E. Gale,et al.  Live-cell delamination counterbalances epithelial growth to limit tissue overcrowding , 2012, Nature.

[31]  J. Brugge,et al.  Outgrowth of Single Oncogene-expressing Cells from Suppressive Epithelial Environments , 2012, Nature.

[32]  H. Guillou,et al.  Spatial organization of the extracellular matrix regulates cell–cell junction positioning , 2012, Proceedings of the National Academy of Sciences.

[33]  Masaya Ikegawa,et al.  Loss of Scribble causes cell competition in mammalian cells , 2012, Journal of Cell Science.

[34]  E. Grasland-Mongrain,et al.  Orientation and polarity in collectively migrating cell structures: statics and dynamics. , 2011, Biophysical journal.

[35]  D. Hanahan,et al.  Hallmarks of Cancer: The Next Generation , 2011, Cell.

[36]  Adam J Engler,et al.  Preparation of Hydrogel Substrates with Tunable Mechanical Properties , 2010, Current protocols in cell biology.

[37]  M. Poujade,et al.  Velocity fields in a collectively migrating epithelium. , 2010, Biophysical journal.

[38]  Guillaume Charras,et al.  Interaction with surrounding normal epithelial cells influences signalling pathways and behaviour of Src-transformed cells , 2010, Journal of Cell Science.

[39]  Jean-Paul Vincent,et al.  Characterization of the interface between normal and transformed epithelial cells , 2009, Nature Cell Biology.

[40]  Cédric Leroy,et al.  Quantitative phosphoproteomics reveals a cluster of tyrosine kinases that mediates SRC invasive activity in advanced colon carcinoma cells. , 2009, Cancer research.

[41]  Mahitosh Mandal,et al.  Epithelial to mesenchymal transition in head and neck squamous carcinoma , 2008, Cancer.

[42]  Charles Rattray,et al.  Themes and variations , 2007, Architectural Research Quarterly.

[43]  P. Chavrier,et al.  Collective migration of an epithelial monolayer in response to a model wound , 2007, Proceedings of the National Academy of Sciences.

[44]  C. Dive,et al.  Increases in c-Src expression level and activity do not promote the growth of human colorectal carcinoma cells in vitro and in vivo. , 2006, Neoplasia.

[45]  J. Gutkind,et al.  VEGF controls endothelial-cell permeability by promoting the β-arrestin-dependent endocytosis of VE-cadherin , 2006, Nature Cell Biology.

[46]  J. Parsons,et al.  Src family kinases, key regulators of signal transduction , 2004, Oncogene.

[47]  Marcel Mettlen,et al.  v-Src accelerates spontaneous motility via phosphoinositide 3-kinase, phospholipase C and phospholipase D, but abrogates chemotaxis in Rat-1 and MDCK cells , 2004, Journal of Cell Science.

[48]  G. Gallick,et al.  Src family kinases in tumor progression and metastasis , 2003, Cancer and Metastasis Reviews.

[49]  E. Avizienyte,et al.  Elevated c-Src is linked to altered cell–matrix adhesion rather than proliferation in KM12C human colorectal cancer cells , 2002, British Journal of Cancer.

[50]  G. McLean,et al.  Src-induced de-regulation of E-cadherin in colon cancer cells requires integrin signalling , 2002, Nature Cell Biology.

[51]  M. Poupon,et al.  Src kinase contributes to the metastatic spread of carcinoma cells , 2002, Oncogene.

[52]  M. T. Brown,et al.  Regulation, substrates and functions of src. , 1996, Biochimica et biophysica acta.

[53]  Frans,et al.  Loss of epithelial differentiation and gain of invasiveness correlates with tyrosine phosphorylation of the E-cadherin/beta-catenin complex in cells transformed with a temperature-sensitive v-SRC gene , 1993, The Journal of cell biology.

[54]  F. Cross,et al.  A short sequence in the p60src N terminus is required for p60src myristylation and membrane association and for cell transformation , 1984, Molecular and cellular biology.

[55]  T. Hunter,et al.  Transforming gene product of Rous sarcoma virus phosphorylates tyrosine , 1980, Proceedings of the National Academy of Sciences.

[56]  R. Erikson,et al.  Protein kinase activity associated with the avian sarcoma virus src gene product. , 1978, Proceedings of the National Academy of Sciences of the United States of America.

[57]  H. Varmus,et al.  DNA related to the transforming gene(s) of avian sarcoma viruses is present in normal avian DNA , 1976, Nature.

[58]  P. Rous.  A SARCOMA OF THE FOWL TRANSMISSIBLE BY AN AGENT SEPARABLE FROM THE TUMOR CELLS , 1911, The Journal of experimental medicine.

[59]  C. Hogan.  Impact of interactions between normal and transformed epithelial cells and the relevance to cancer , 2011, Cellular and Molecular Life Sciences.

[60]  M. Piel,et al.  Protein micropatterns: A direct printing protocol using deep UVs. , 2010, Methods in cell biology.

[61]  T. Deramaudt,et al.  Src activation and translocation from focal adhesions to membrane ruffles contribute to formation of new adhesion sites , 2008, Cellular and Molecular Life Sciences.

[62]  G. Collins.  The next generation. , 2006, Scientific American.

[63]  D. Larson,et al.  Csk-deficient boundary cells are eliminated from normal Drosophila epithelia by exclusion, migration, and apoptosis. , 2006, Developmental cell.

[64]  S. Parsons,et al.  c-Src, receptor tyrosine kinases, and human cancer. , 1999, Advances in cancer research.