Scatter factor is a fibroblast-derived modulator of epithelial cell mobility

Stoker, M. G. P.; Gherardi, Ermanno; Perryman, M. Benjamin; Gray, Julia

doi:10.1038/327239a0

Cited by 1,256 publications

(806 citation statements)

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“…Despite its biological relevance, the molecular mechanism responsible for cell migration are still only partially understood. Recent studies had identi®ed actin polymerization and depolymerization as crucial events (Cooper, 1991), and have showed that these processes are regulated by extracellular factors, such as HGF and LPA (Stoker et al, 1987;Hordijk et al, 1994). Although BAG-1 promotes HGF-mediated growth and anti-apoptotic signaling (Bardelli et al, 1996), in our study, no signi®cant di erence among the MKN74 transfectants was observed with regards to migratory responses to HGF.…”

Section: Discussionmentioning

confidence: 99%

“…BAG-1 has been reported to associate with the HGF (scatter factor) receptor, a growth factor receptor which is known to promote cell motility (Stoker et al, 1987), which is sometimes overexpressed in gastric cancers (Di Renzo et al, 1991). To examine the potential role of BAG-1 in promoting cell migration, the MKN74 transfectants were analysed by goldparticle colloid assay with or without FBS or HGF as described previously (Takaoka et al, 1997).…”

Section: Bag-1 Overexpression Promotes Mkn74 Cell Migrationmentioning

confidence: 99%

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BAG-1 accelerates cell motility of human gastric cancer cells

et al. 1999

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Section: Discussionmentioning

confidence: 99%

Section: Bag-1 Overexpression Promotes Mkn74 Cell Migrationmentioning

confidence: 99%

BAG-1 accelerates cell motility of human gastric cancer cells

et al. 1999

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“…There is some evidence for a pivotal role of HGF in the regulation of the cell motility, and as a mitogen and motogen for certain epithelial cells and vascular endothelial cells in culture (Stoker et al, 1987;Rosen et al, 1990a). HGF prevented loss of cell viability and morphological damage and retarded DNA fragmentation in confluent C2.8 cells (Rovoltella et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have suggested that HGF is produced by non-parenchymal hepatic cells including Kupffer cells (Noji et al, 1990), endothelial cells (Stoker et al, 1987;Shima et al, 1991), fibroblasts and fat-storing cells in the liver (Ramadori et al, 1992;Schirmacher et al, 1992), endothelial cells in the lung Yanagita et al, 1992). Experimentally, tumour cells are also known to produce HGF; HGF or mRNA encoding this factor has been detected in fibrosarcoma (Stoker et al, 1987), lung cancer (Yoshinaga et al, 1992;Rygaard et al, 1993;Tsao et al, 1993); hepatoma (Miyazaki et al, 1991) and pancreatic cancer cells (Hirota et al, 1993). Other normal tissues, such as the pancreas, small intestine, thyroid, brain and submaxillary salivary gland are also known to produce HGF (Zarmegar et al, 1990;Wolf et al, 1991).…”

Section: Methodsmentioning

confidence: 99%

Serum hepatocyte growth factor as an index of disease status of patients with colorectal carcinoma

Fukuura

Miki²,

Inoue³

et al. 1998

Br J Cancer

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Summary To evaluate the clinical significance of serum levels of hepatocyte growth factor (HGF) in colorectal cancer patients, we measured the venous and portal concentrations of HGF in 60 patients. The tissue concentrations in the tumour and adjacent normal mucosa were also determined. The serum HGF concentration for the peripheral venous blood of the patients was significantly higher than that in normal controls. The content of HGF in cancer tissue was also significantly higher than that in normal mucosa, and it was correlated with the serum HGF concentration for the peripheral venous blood. The serum concentration of HGF reflected pathological features, including tumour size and lymph node or liver metastasis, and it showed an association with various preoperative nutritional parameters and the preoperative haemoglobin level. The serum HGF concentration was also correlated with the serum concentrations of immunosuppressive acidic protein and interleukin-6, indices of the host's immunological condition. Serum HGF seems to be a useful index of the disease status of patients with colorectal carcinoma.Keywords: hepatocyte growth factor; nutritional status; immunological status; colorectal cancer Hepatocyte growth factor (HGF) is a multifunctional cytokine that is the most potent known stimulator of hepatocyte growth and DNA synthesis Kaneko et al, 1992). HGF has also been recognized as a tumour-disseminating factor (Weidner et al, 1991;Mayer et al, 1993;Tannapfel et al, 1994). In several experimental studies, evidence has been acquired of a relation of HGF to the progression of tumour cells . Among the particularly important biological activities of HGF in tumour cells is its capacity to increase epithelial cell proliferation and motility (Gherardi et al, 1990). In clinical studies, a relationship between the concentration of HGF in serum or cancer tissue and the progression of disease has been noted in patients with gastric cancer (Taniguchi et al, 1997), oesophageal cancer (Takada et al, 1995) and breast cancer (Yamashita et al, 1994;Taniguchi et al, 1995). However, there are no reports regarding the clinical relevance of HGF in patients with colorectal carcinoma.Malnutrition or immunosuppression are involved in the development of life-threatening complications in patients with malignancies (Braga et al, 1988;Nishi et al, 1988;Dannhauser et al, 1995;Triantafillidis et al, 1995;Windsor et al, 1995;Goransson et al, 1996). Patients with advanced cancer and cachexia typically demonstrate modestly increased rates of energy expenditure with concomitant diminished food intake. These metabolic changes may be due to mediators released by the tumour or by the host (Keller, 1993). Recently, the role of cytokines in these metabolic changes was emphasized (Gambardella et al, 1997). In addition, the relationship between cytokines and an immunosuppressive substance has also been highlighted (Tanaka et al, 1993 The objective of this study was to evaluate the relationship between serum HGF concentration and clinicopathological ...

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“…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). MET function is required for various morphogenetic events in both embryonic and adult life 21,22 and it drives the malignant progression of several different types of tumours 23 .…”

Section: Introductionmentioning

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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Scatter factor is a fibroblast-derived modulator of epithelial cell mobility

Cited by 1,256 publications

References 0 publications

BAG-1 accelerates cell motility of human gastric cancer cells

BAG-1 accelerates cell motility of human gastric cancer cells

Serum hepatocyte growth factor as an index of disease status of patients with colorectal carcinoma

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

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