Activation of NF-κB Is Essential for Hepatocyte Growth Factor-Mediated Proliferation and Tubulogenesis

Müller, Markus; Morotti, Alessandro; Ponzetto, Carola

doi:10.1128/mcb.22.4.1060-1072.2002

Cited by 117 publications

(92 citation statements)

References 83 publications

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“…Thus, HGF/ SF stimulated NF-kB signaling in a liver cell line (MLP29), and inhibition of NF-kB blocked HGF/ SF-induced proliferation and tubulogenesis, but not scattering (Muller et al, 2002). However, NF-kB was not required for the antiapoptotic function of HGF/SF.…”

Section: Discussionmentioning

confidence: 99%

Role of NF-κB signaling in hepatocyte growth factor/scatter factor-mediated cell protection

et al. 2005

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Section: Discussionmentioning

confidence: 99%

Role of NF-κB signaling in hepatocyte growth factor/scatter factor-mediated cell protection

et al. 2005

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“…At the signalling level, the series of events required for HGF-dependent tubule formation has been dissected. As a whole, this process requires the integrity of the STAT3 and NF-κB pathways 47,77 . The initial EMT relies on hypersustained activation of the Raf-MEK-ERK pathway, which, as discussed earlier, is triggered by the association of active MET-bound GAB1 with the tyrosine phosphatase SHP2 (Refs 44,53,118,119).…”

Section: Met Signalling In Development and Diseasementioning

confidence: 99%

“…In response to MET, IKK activation is mediated by the PI3K-Akt pathway and Src as signalling intermediates, but the direct distal effectors of IKK stimulation are unknown 76 . IKKinduced destruction of IκBs leads to the release of NF-κB, which translocates to the nucleus to stimulate the transcription of various genes, including mitogenic and anti-apoptotic regulators 76,77 (Fig. 2d).…”

mentioning

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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“…1774425; Roche), as previously described [17]. One essential feature of apoptosis is the fragmentation of DNA, because of the activation of endonucleases.…”

Section: Cell Death Enzyme-linked Immunosorbent Assaymentioning

confidence: 99%

NF‐kB inhibition as a strategy to enhance etoposide‐induced apoptosis in K562 cell line

et al. 2006

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Activation of NF-κB Is Essential for Hepatocyte Growth Factor-Mediated Proliferation and Tubulogenesis

Cited by 117 publications

References 83 publications

Role of NF-κB signaling in hepatocyte growth factor/scatter factor-mediated cell protection

Role of NF-κB signaling in hepatocyte growth factor/scatter factor-mediated cell protection

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

NF‐kB inhibition as a strategy to enhance etoposide‐induced apoptosis in K562 cell line

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