Regulation of matrix metalloproteinase-2 (MMP-2) by hepatocyte growth factor/scatter factor (HGF/SF) in human glioma cells: HGF/SF enhances MMP-2 expression and activation accompanying up-regulation of membrane type-1 MMP

Hamasuna, Ryouichi; Kataoka, Hiroaki; Moriyama, Takuzou; Itoh, Hiroshi; Seiki, Motoharu; Koono, Masashi

doi:10.1002/(sici)1097-0215(19990719)82:2<274::aid-ijc19>3.0.co;2-2

Cited by 72 publications

(41 citation statements)

References 34 publications

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“…It has been shown to be highly expressed in high grade bladder tumours using immunohistochemistry (Neal et al, 1990). The Hepatocyte Growth Factor (HGF) receptor c-MET tyrosine kinase is expressed on epithelially derived tumour cells, and is involved in HGF mediated activation of both MMP2 and MT1-MMP (Hamasuna et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Comprehensive profiling and localisation of the matrix metalloproteinases in urothelial carcinoma

et al. 2006

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The matrix metalloproteinases (MMPs) are endopeptidases which break down the extracellular matrix and regulate cytokine and growth factor activity. Several MMPs have been implicated in the promotion of invasion and metastasis in a broad range of tumours including urothelial carcinoma. In this study, RNA from 132 normal bladder and urothelial carcinoma specimens was profiled for each of the 24 human MMPs, the four endogenous tissue inhibitors of MMPs (TIMPs) and several key growth factors and their receptors using quantitative real time RT -PCR. Laser capture microdissection (LCM) of RNA from 22 tumour and 11 normal frozen sections was performed allowing accurate RNA extraction from either stromal or epithelial compartments. This study confirms the over expression in bladder tumour tissue of well-documented MMPs and highlights a range of MMPs which have not previously been implicated in the development of urothelial cancer. In summary, MMP-2, MT1-MMP and the previously unreported MMP-28 were very highly expressed in tumour samples while MMPs 1, 7, 9, 11, 15, 19 and 23 were highly expressed. There was a significant positive correlation between transcript expression and tumour grade for MMPs 1, 2, 8, 10, 11, 12, 13, 14, 15 and 28 (Po0.001). At the same confidence interval, TIMP-1 and TIMP-3 also correlated with increasing tumour grade. LCM revealed that most highly expressed MMPs are located primarily within the stromal compartment except MMP-13 which localised to the epithelial compartment. This work forms the basis for further functional studies, which will help to confirm the MMPs as potential diagnostic and therapeutic targets in early bladder cancer.

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Section: Discussionmentioning

confidence: 99%

Comprehensive profiling and localisation of the matrix metalloproteinases in urothelial carcinoma

et al. 2006

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“…Moreover, several investigators reported that HGF up-regulated matrix-degrading enzymes. [31][32][33][34] We also reported that the augmentation of HGF/c-met signal upregulated proMMP9, proMMP1, and uPA in a renal cell carcinoma cell line, Caki-1. 18 In this oral SCC cell system, we also examined the effect of HGF on the activity of the gelatinase produced by BHY and HN cells.…”

Section: Discussionmentioning

confidence: 99%

Role of HGF/c-met system in invasion and metastasis of oral squamous cell carcinoma cellsin vitro and its clinical significance

et al. 2001

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We examined the role of the hepatocyte growth factor (HGF)/c-met system on invasion and metastasis of oral squamous cell carcinoma (SCC) cells. In monolayer culture, exogenous HGF marginally affected the growth of oral SCC cells (BHY, HN, IH) and human gingival epithelial cells (GE). In type I collagen matrix, however, HGF significantly enhanced the invasive growth of the cancer cells (p < 0.05). We detected the expression of c-met (HGF receptor) mRNA in all of the cancer cells, but not in human gingival fibroblasts (GF). Oral SCC cells did not secret HGF protein into the medium, but GF secreted a large amount of HGF protein (15 ng/ml). Furthermore, HGF markedly enhanced the migration of cancer cells in a Transwell invasion chamber. Then, we examined the serum levels of HGF in oral SCC patients, or HGF concentrations in oral cancer tissues. Serum levels of HGF in the patients were significantly higher than those in healthy volunteers (p < 0.05). After initial treatment, all of the tumor-free survivors showed a marked decline in the serum HGF levels. Furthermore, HGF concentrations in metastatic cancer tissues were significantly higher than those of nonmetastatic cancer tissues and normal gingiva (p < 0.01). These results suggest that HGF plays an important role in invasion and metastasis of oral SCC cells as a paracrine factor, and an elevated HGF level in the cancer tissue can be a predictive marker for metastasis formation in patients with oral SCC. © 2001 Wiley-Liss, Inc. Key words: oral SCC; HGF; c-met; metastasisOral SCCs are characterized by a high degree of local invasion and a high rate of metastases to cervical lymph nodes, but a low rate of metastases to distant organs. Moreover, oral SCC frequently show local recurrence after initial treatment, probably due to micro-invasion or micro-metastasis of the tumor cells at the primary site. We recently reported that oral SCC cells produced a large amount of matrix-degrading enzymes and that the net activity of MMP2 (active-MMP2/TIMP2) produced by cancer cells contributes to lymph-node metastasis in a nude-mouse orthotopic inoculation model. 1 We also noted that cancer cells in the peripheral blood of patients with oral SCC were frequently detected by RT-PCR for cytokeratin 20 mRNA, and that there was no clear relationship between the hematogenous cancer cells and the metastasis. 2 Furthermore, by microdissection zymography, we demonstrated that active MMP2 in cancer cell nests could be a predictive marker for metastasis formation in patients with oral SCC. 3 The precise molecular mechanisms of invasion and metastasis of oral cancer, however, especially the interaction between cancer cells and host cells, are still unknown.

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“…Moreover, intramyocardial delivery of HGF in mice enhanced migration of c-kit þ CSCs from surrounding myocardium to the infarcted region where they formed new myocytes and improved cardiac contractile function . Interestingly, the effect of HGF on migration of c-kit þ CSCs has been attributed to the expression of matrix metalloproteinases (Hamasuna et al, 1999;Urbanek et al, 2005).…”

Section: Hepatocyte Growth Factor/c-metmentioning

confidence: 99%

Migration of Resident Cardiac Stem Cells in Myocardial Infarction

Liang

Phillips

2012

The Anatomical Record

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Ischemic heart disease is a major cause of morbidity and mortality worldwide. Stem cell-based therapy, which aims to restore cardiac structure and function by regeneration of functional myocardium, has recently been proposed as a novel alternative treatment modality. Resident cardiac stem cells (CSCs) in adult hearts are a key cell type under investigation. CSCs have been shown to be able to repair damaged myocardium and improve myocardial function in both human and animal studies. This approach relies not only on the proliferation of the CSCs, but also upon their migration to the site of injury within the heart. Here, we briefly review reported CSC populations and discuss signaling factors and pathways required for the migration of CSCs. Anat Rec, 296:184-191, 2013. V C 2012 Wiley Periodicals, Inc.

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Regulation of matrix metalloproteinase-2 (MMP-2) by hepatocyte growth factor/scatter factor (HGF/SF) in human glioma cells: HGF/SF enhances MMP-2 expression and activation accompanying up-regulation of membrane type-1 MMP

Cited by 72 publications

References 34 publications

Comprehensive profiling and localisation of the matrix metalloproteinases in urothelial carcinoma

Comprehensive profiling and localisation of the matrix metalloproteinases in urothelial carcinoma

Role of HGF/c-met system in invasion and metastasis of oral squamous cell carcinoma cellsin vitro and its clinical significance

Migration of Resident Cardiac Stem Cells in Myocardial Infarction

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