The biological role of HGF-MET axis in tumor growth and development of metastasis

Lesko, Ewa; Majka, Marcin

doi:10.2741/2760

Cited by 97 publications

(72 citation statements)

References 71 publications

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“…HGF has been shown to stimulate endothelial cell proliferation and survival, and acts as a pro-angiogenic molecule [79]. HGF is involved in tumoral angiogenesis and metastasis [80,81]. In addition, HGF is synthesized by myeloma cells [82] and enhances MMP-9 secretion by myeloma cells [83].…”

Section: Matrix Metalloproteinasesmentioning

confidence: 99%

Angiogenesis and Multiple Myeloma

Giuliani

Storti

Bolzoni

et al. 2011

Cancer Microenvironment

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The bone marrow microenvironment in multiple myeloma is characterized by an increased microvessel density. The production of pro-angiogenic molecules is increased and the production of angiogenic inhibitors is suppressed, leading to an "angiogenic switch". Here we present an overview of the role of angiogenesis in multiple myeloma, the pro-angiogenic factors produced by myeloma cells and the microenvironment, and the mechanisms involved in the myeloma-induced angiogenic switch. Current data suggest that the increased bone marrow angiogenesis in multiple myeloma is due to the aberrant expression of angiogenic factors by myeloma cells, the subsequent increase in pro-angiogenic activity of normal plasma cells as a result of myeloma cell angiogenic activity, and the increased number of plasma cells overall. Hypoxia also contributes to the angiogenic properties of the myeloma marrow microenvironment. The transcription factor hypoxia-inducible factor-1α is overexpressed by myeloma cells and affects their transcriptional and angiogenic profiles. In addition, potential roles of the tumor suppressor gene inhibitor of growth family member 4 and homeobox B7 have also been recently highlighted as repressors of angiogenesis and pro-angiogenic related genes, respectively. This complex pathogenetic model of myeloma-induced angiogenesis suggests that several proangiogenic molecules and related genes in myeloma cells and the microenvironment are potential therapeutic targets.

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Section: Matrix Metalloproteinasesmentioning

confidence: 99%

Angiogenesis and Multiple Myeloma

Giuliani

Storti

Bolzoni

et al. 2011

Cancer Microenvironment

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“…18,19 HGF is an antifibrotic factor and has potential use in treating chronic renal failure by promoting transdifferentiation and proliferation of tubular epithelial cells. 20 HGF and TGF-b1 are in a dynamic balance in normal tissues, but this balance is lost in morbid tissues. If the balance favors HGF, repair of damaged tissues is promoted.…”

Section: Discussionmentioning

confidence: 99%

Pathological changes, TGF-β1 expression, and the effects of hepatocyte growth factor in 5/6 nephrectomized rats

Wang

Yang

et al. 2013

Renal Failure

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Several studies have shown that hepatocyte growth factor (HGF) ameliorates chronic renal failure, but its mechanism of action is unclear. This study was designed to test the delivery of HGF in the PCI-neo vector, using the 5/6 nephrectomized rat as a model for chronic renal failure, and to confirm that this protective function is associated with decreased protein expression of transforming growth factor-beta1 (TGF-b1). Rats were randomly divided into the following groups: Control (untreated), PCI-neo (vector control), 5/6 nephrectomy, and PCI-neo-HGF. Rats were sacrificed at both the fifth and ninth week after 5/6 nephrectomy. Kidney specimens were used for pathological examination (hematoxylin-eosin staining), and detection of TGF-b1 protein (Western blot and immunohistochemistry) expression. Blood urea nitrogen, serum creatinine, and 24-h urinary protein excretion (UPE) were increased, renal interstitium was seriously injured, and TGF-b1 protein expression was elevated in 5/6 nephrectomized rats compared to control rats at either time point. Red blood cell and hemoglobin levels decreased in the ninth week after 5/6 nephrectomy. PCI-neo-HGF expression ameliorated the aforementioned changes and decreased TGF-b1 expression, not only in the fifth week, but also in the ninth week after surgery. The process of renal injury in the 5/6 nephrectomized rat was consistent with that of chronic renal failure. The increase in TGF-b1 expression was maintained after 5/6 nephrectomy. HGF relieved chronic renal failure, this protection was associated with down-regulation of TGF-b1 protein expression, and the protective effects were long-term and stable after 5/6 nephrectomy.Keywords 5/6 nephrectomized rats, hepatocyte growth factor, pathological changes, PCI-neo, transforming growth factor-b1History

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“…For this cell line, cell scattering involves not only the loss of most intercellular junctions (but not all) and the dissociation of the cells from the epithelial layer, but also a cytoskeletal reorganization followed by an active migration [9,21,13]. Moreover the addition of the HGF induces cell polarization, forma-tion of branched tubules and makes the cellular colonies assume a stellar-shape configurations (see Fig.…”

Section: Introduction and Phenomenological Descriptionmentioning

confidence: 99%

Individual cell-based models of cell scatter of ARO and MLP-29 cells in response to hepatocyte growth factor

Scianna

Merks

Preziosi

et al. 2009

Journal of Theoretical Biology

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The different behaviours of colonies of two cell lines, ARO and MLP-29, in response to Hepatocyte Growth Factor (HGF) are described deducing suitable Cellular Potts Model (CPM). It is shown how increased motility and decreased adhesiveness are responsible for cellcell dissociation and tissue invasion in the ARO cells. On the other hand, it is shown that, in addition to the biological mechanisms above, it is necessary to include cell persistence in motion and HGF diffusion to describe the scattering and the branching processes characteristic of MLP-29 cells.

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The biological role of HGF-MET axis in tumor growth and development of metastasis

Cited by 97 publications

References 71 publications

Angiogenesis and Multiple Myeloma

Angiogenesis and Multiple Myeloma

Pathological changes, TGF-β1 expression, and the effects of hepatocyte growth factor in 5/6 nephrectomized rats

Individual cell-based models of cell scatter of ARO and MLP-29 cells in response to hepatocyte growth factor

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