Met receptor signaling is required for sensory nerve development and HGF promotes axonal growth and survival of sensory neurons

Maina, Flavio; Hilton, Mark; Ponzetto, Carola; Davies, Alun M.; Klein, Rüdiger

doi:10.1101/gad.11.24.3341

Cited by 218 publications

(180 citation statements)

References 39 publications

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“…This is consistent with HGF/SF acting as a potent mitogen for hepatocytes in vivo and the important role of Met in liver regeneration (Borowiak et al, 2004;Huh et al, 2004). In addition, these studies have demonstrated a role for Met and HGF/SF for the directional migration of myoblasts from the somites of the limbs and in the development and innervation of skeletal muscles, and directing the growth of axonal cones (Schmidt et al, 1995;Uehara et al, 1995;Yang and Park, 1995;Ebens et al, 1996;Maina et al, 1997).…”

Section: Met and Hgf/sf Elicit A Program Of Proliferative And Invasivsupporting

confidence: 66%

From Tpr-Met to Met, tumorigenesis and tubes

2007

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The receptor for hepatocyte growth factor (HGF)/scatter factor (SF), Met, controls a program of invasive epithelial growth through the coordination of cell proliferation and survival, cell migration and epithelial morphogenesis. This process is important during embryogenesis and for organ regeneration in the adult. However, when deregulated the HGF/SF-Met signaling axis contributes to tumorigenesis and metastasis. Studies on the oncogenic activation of the Met receptor have shed light on the molecular mechanisms underlying the oncogenic activation of receptor tyrosine kinase (RTKs). More than a decade ago, work on the Met related oncogene, Tpr-Met, revealed the mechanism for activation of RTK-derived oncogenes generated following chromosomal translocation. More recently, studies on the mechanisms of downregulation of the Met RTK highlight a role for loss of downregulation in RTK oncogenic activation.

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Section: Met and Hgf/sf Elicit A Program Of Proliferative And Invasivsupporting

confidence: 66%

From Tpr-Met to Met, tumorigenesis and tubes

2007

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“…Ablation of the Hgf or Met genes results in complete absence of this specific muscle type, leaving all other muscle groups unaffected 104,105,106 . Finally, disruption of HGF-MET function affects the proper wiring of the nervous system, leading to reduced survival of sensory and sympathetic neurons as well as impaired outgrowth and fasciculation (axon bundling) of certain motor nerves 110,111,112 .…”

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

1,058

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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“…In normal physiology, these signaling pathways promote activation of cytoplasmic and nuclear processes, which lead to a variety of cellular functions, including proliferation and protection from apoptosis (8)(9)(10). The MET pathway also mediates functions such as wound healing and hepatic regeneration, and has pivotal roles in normal liver development (11), embryonic placental development, and the formation of muscle and neurons (12)(13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

MET in Lung Cancer: Biomarker Selection Based on Scientific Rationale

Salgia

2017

Molecular Cancer Therapeutics

129

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MET or hepatocyte growth factor (HGF) receptor pathway signaling mediates wound healing and hepatic regeneration, with pivotal roles in embryonic, neuronal, and muscle development. However, dysregulation of MET signaling mediates proliferation, apoptosis, and migration and is implicated in a number of malignancies. In non-small cell lung cancer (NSCLC), aberrant MET signaling can occur through a number of mechanisms that collectively represent a significant proportion of patients. These include MET or HGF protein overexpression, MET gene amplification, MET gene mutation or fusion/rearrangement, or aberrations in downstream signaling or regulatory components. Responses to MET tyrosine kinase inhibitors have been documented in clinical trials in patients with MET-amplified or METoverexpressing NSCLC, and case studies or case series have shown that MET mutation/deletion is a biomarker that is also predictive of response to these agents. However, other recent clinical data have highlighted an urgent need to elucidate optimal biomarkers based on genetic and/or protein diagnostics to correctly identify patients most likely to benefit in ongoing clinical trials of an array of MET-targeted therapies of differing class. The latest advances in the development of MET biomarkers in NSCLC have been reviewed, toward establishing appropriate MET biomarker selection based on a scientific rationale. Mol Cancer Ther; 16(4); 555-65.Ó2017 AACR.

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Met receptor signaling is required for sensory nerve development and HGF promotes axonal growth and survival of sensory neurons

Cited by 218 publications

References 39 publications

From Tpr-Met to Met, tumorigenesis and tubes

From Tpr-Met to Met, tumorigenesis and tubes

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

MET in Lung Cancer: Biomarker Selection Based on Scientific Rationale

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