How to make tubes: signaling by the Met receptor tyrosine kinase

Rosário, Marta

doi:10.1016/s0962-8924(03)00104-1

Cited by 232 publications

(189 citation statements)

References 76 publications

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“…When embedded in a collagen matrix, normal epithelial cells proliferate and assemble into spheroids, which feature a centrally localized, hollow lumen, surrounded by polarized cells 116 . HGF causes spheroids to form elongated tubules in a stepwise sequence of biological events 117 . First, cells undergo a partial epithelial-mesenchymal transition (EMT), which involves the transformation of tightly packed elements into invasive, spindle-shaped cells that emit long cytoplasmic extensions in the surrounding matrix.…”

Section: Met Signalling In Development and Diseasementioning

confidence: 99%

MET signalling: principles and functions in development, organ regeneration and cancer

Trusolino

Bertotti

Comoglio

2010

Nat Rev Mol Cell Biol

1,083

1,076

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The MET tyrosine kinase receptor (also known as the HGF receptor) promotes tissue remodelling, which underlies developmental morphogenesis, wound repair, organ homeostasis and cancer metastasis, by integrating growth, survival and migration cues in response to environmental stimuli or cell-autonomous perturbations. The versatility of MET-mediated biological responses is sustained by qualitative and quantitative signal modulation. Qualitative mechanisms include the engagement of dedicated signal transducers and the subcellular compartmentalization of MET signalling pathways, whereas quantitative regulation involves MET partnering with adaptor amplifiers or being degraded through the shedding of its extracellular domain or through intracellular ubiquitylation. Controlled activation of MET signalling can be exploited in regenerative medicine, whereas MET inhibition might slow down tumour progression.Throughout embryogenesis, cells bud off from developing tissues and move outwards to shape and pattern the complex architecture of prospective organs 1 . A similar process occurs in adult life during wound healing and tissue repair, when lingering cells migrate into injury sites to recreate the pre-existing structures 2 . The acquisition of cell motility is necessary, but not sufficient, for this event. Cells that detach from their neighbours must elude anoikis, a form of apoptotic cell death that occurs when cells lose adhesion with the extracellular matrix 3 . Moreover, migratory cells undergo extensive mitotic divisions to produce 'founder populations', which settle in newly forming organs during development or colonize worn tissues during repair 4,5 . The normal phases of embryogenesis and organ regeneration strongly resemble the pathological process of tumour invasiveness: similarly to cells at the wound edge, cells at the tumour's leading front disrupt intercellular contacts and infiltrate the adjacent surroundings, where they resist anoikis and grow before lodging in the blood vessels for systemic dissemination 6 . This resemblance is not simply a biological correlate, it has a common mechanistic basis: cancer cells resurrect the latent schemes of cellular reorganization, which are usually confined to embryonic development and damaged adult organs, and leverage them to become competent for metastasization 7 . The activities -motility, survival and proliferation -that occur in developing, injured and neoplastic tissues embody a biological programme that is defined as 'invasive growth' 8 . This is triggered by extracellular stimuli that regulate the activity of several transcription factors that, in turn, modulate the expression of a number of proteins, ranging from cytoskeletal and cell-cell junctional components to cell cycle regulators and anti-apoptotic effectors 9, 10 . One major environmental inducer of invasive growth is hepatocyte growth factor (HGF, also known as scatter factor), the ligand for the MET tyrosine kinase receptor (also known as the HGF receptor) 11,12,13,14,15,16,17,18,19,20 (Box 1). ...

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Section: Met Signalling In Development and Diseasementioning

confidence: 99%

MET signalling: principles and functions in development, organ regeneration and cancer

Trusolino

Bertotti

Comoglio

2010

Nat Rev Mol Cell Biol

1,083

1,076

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“…A second process of tube formation involves the migration of individual cells from an epithelial structure and their subsequent rearrangement to form a hollow tube, as exemplified by the formation of vascular systems in vivo [6][7][8] or tubules derived from renal epithelial cells grown in vitro [9,10]. In this case, migrating cells remain attached to each other to form a chain and eventually a cord of cells, from which a central lumen space contiguous along the length of the cord is generated to form a tube.…”

Section: Formation Of a Tube -So Many Possibilitiesmentioning

confidence: 99%

“…Rosario and Birchmeier [10] discussed the roles of another growth factor-receptor signaling pathway comprising HGF and its receptor Met, which has been implicated in stimulating the formation and outgrowth of epithelial tubes [9,10]; in addition, downstream targets of this signaling pathway have been described in detail (see below). However, the loss of function of HGF or Met does not cause kidney abnormalities showing that the HGFMet pathway works with, or is redundant to, other growth-factor signaling pathways [10]. Little is understood about mesenchyme to epithelium conversion that gives rise to the nephron tubule.…”

Section: Localized Growth Factors Directional Cues and Receptorsmentioning

confidence: 99%

“…Although many pathways involving growth-factor receptors participate in the induction of tube elongation and migration (see above), in most cases little is known about their downstream effector pathways. As noted by Rosario and Birchmeier [10] and by Mostov and colleagues [9], an exception is HGF-Met signaling in which HGF binding to its receptor met leads to the recruitment of a complex of signaling proteins to Met, which in turn regulates the dissociation of adherens junctions and stimulates cell motility, proliferation and morphogenesis.…”

Section: Forming Tubes: Downstream Effectors Of Master Regulators Andmentioning

confidence: 99%

“…The review articles in Tube Morphogenesis Series in Trends in Cell Biology [4][5][6][7][8][9][10][11][12][13][14][15][16] reveal many potential parallels in the molecular controls that define decisions on cell fate and cue morphogenetic movements during tube formation, cellular rearrangements and instructional cell-cell/cell-ECM interactions involved in the formation of tubes. Many gaps remain, however, and it is not yet possible to construct a complete picture of tube formation in one system, from master transcriptional regulators and induction of cell differentiation to mechanisms of cell outgrowth and dynamics of migration.…”

Section: Concluding Remarks -Closure But Many Openings Remainmentioning

confidence: 99%

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Tube morphogenesis: closure, but many openings remain

Nelson

2003

Trends in Cell Biology

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3‐phosphoinositide‐dependent protein kinase 1 (PDK1) mediates crosstalk between Src and Akt pathways in MET receptor signaling

et al. 2021

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The high-affinity tyrosine kinase receptor MET plays a pivotal role in several facets of cell regulation. Although its mitogenic effect is well documented, some aspects of connection patterns between signaling pathways involved in cell cycle progression remain to be deciphered. We have used a tractable heterologous expression system, the Xenopus oocyte, to detect connections between distinct MET signaling cascades involved in G2/M progression. Our results reveal that Src acts as an adapter via its SH2 domain to recruit 3phosphoinositide-dependent protein kinase 1 (PDK1) to the MET signaling complex leading to Akt phosphorylation. These data define an original crosstalk between Src and Akt signaling pathways that contributes to METinduced entry into the M phase, and deserves further investigation in pathologies harboring deregulation of this receptor.

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How to make tubes: signaling by the Met receptor tyrosine kinase

Cited by 232 publications

References 76 publications

MET signalling: principles and functions in development, organ regeneration and cancer

MET signalling: principles and functions in development, organ regeneration and cancer

Tube morphogenesis: closure, but many openings remain

3‐phosphoinositide‐dependent protein kinase 1 (PDK1) mediates crosstalk between Src and Akt pathways in MET receptor signaling

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