Matrix metalloproteinase-2 and -9 in the sera and in the urine of human oncocytoma and renal cell carcinoma

Carlo, Angelina Di

doi:10.3892/or.2012.1864

Cited by 28 publications

(22 citation statements)

References 21 publications

(16 reference statements)

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“…In renal cell carcinoma using a zymography technique, it has been shown that MMP-9 levels were higher in the serums from clear cell carcinoma in comparison to levels from oncocytoma patients. The prevailing enhanced MMP-9 lytic activity was abundantly present in clear cell carcinoma, whereas MMP-2 activity values were detected in far lesser concentrations [190]. These results were further confirmed by the same author in a study where MMP-9 levels were increased in the clear cell carcinoma patients versus the oncocytoma patients.…”

Section: Gelatinases (Mmp-2 Mmp-9)supporting

confidence: 77%

Matrix Metalloproteinases in Renal Diseases: A Critical Appraisal

Zakiyanov

Kalousová

Zima

et al. 2019

Kidney Blood Press Res

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Matrix metalloproteinases (MMPs) are endopeptidases within the metzincin protein family that not only cleave extracellular matrix (ECM) components, but also process the non-ECM molecules, including various growth factors and their binding proteins. MMPs participate in cell to ECM interactions, and MMPs are known to be involved in cell proliferation mechanisms and most probably apoptosis. These proteinases are grouped into six classes: collagenases, gelatinases, stromelysins, matrilysins, membrane type MMPs, and other MMPs. Various mechanisms regulate the activity of MMPs, inhibition by tissue inhibitors of metalloproteinases being the most important. In the kidney, intrinsic glomerular cells and tubular epithelial cells synthesize several MMPs. The measurement of circulating MMPs can provide valuable information in patients with kidney diseases. They play an important role in many renal diseases, both acute and chronic. This review attempts to summarize the current knowledge of MMPs in the kidney and discusses recent data from patient and animal studies with reference to specific diseases. A better understanding of the MMPs’ role in renal remodeling may open the way to new interventions favoring deleterious renal changes in a number of kidney diseases.

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Section: Gelatinases (Mmp-2 Mmp-9)supporting

confidence: 77%

Matrix Metalloproteinases in Renal Diseases: A Critical Appraisal

Zakiyanov

Kalousová

Zima

et al. 2019

Kidney Blood Press Res

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“…As a family of zinc-containing endopeptidases, matrix metalloproteinases (MMPs) are the major enzymes involved in ECM degradation [30,31]. Two representative members, MMP-2 and MMP-9, were reported highly expressed in invasive tumours [32,33]. The expression of MMP-2 and MMP-9 was reduced after re-expression of DACH1 in GC cells, and this relationship was confirmed by knocking down DACH1 in GES-1 cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

Epigenetic silencing of DACH1 induces the invasion and metastasis of gastric cancer by activating TGF‐β signalling

Herman

et al. 2014

J Cellular Molecular Medi

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Gastric cancer (GC) is the fourth most common malignancy in males and the fifth most common malignancy in females worldwide. DACH1 is frequently methylated in hepatic and colorectal cancer. To further understand the regulation and mechanism of DACH1 in GC, eight GC cell lines, eight cases of normal gastric mucosa, 98 cases of primary GC and 50 cases of adjacent non-tumour tissues were examined. Methylation-specific PCR, western blot, transwell assay and xenograft mice were used in this study. Loss of DACH1 expression correlated with promoter region methylation in GC cells, and re-expression was induced by 5-Aza-2′-deoxyazacytidine. DACH1 is methylated in 63.3% (62/98) of primary GC and 38% (19/50) of adjacent non-tumour tissues, while no methylation was found in normal gastric mucosa. Methylation of DACH1 correlated with reduced expression of DACH1 (P < 0.01), late tumour stage (stage III/IV) (P < 0.01) and lymph node metastasis (P < 0.05). DACH1 expression inhibited epithelial–mesenchymal transition and metastasis by inhibiting transforming growth factor (TGF)-β signalling and suppressed GC cell proliferation through inducing G2/M phase arrest. The tumour size is smaller in DACH1-expressed BGC823 cell xenograft mice than in unexpressed group (P < 0.01). Restoration of DACH1 expression also sensitized GC cells to docetaxel. These studies suggest that DACH1 is frequently methylated in human GC and expression of DACH1 was controlled by promoter region methylation. DACH1 suppresses GC proliferation, invasion and metastasis by inhibiting TGF-β signalling pathways both in vitro and in vivo. Epigenetic silencing DACH1 may induce GC cells' resistance to docetaxel.

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“…Particularly, the high expression of MMP-9 is considered as a crucial factor for cell migration/invasion of endothelial cells into the adjacent stroma (30). It is essential to elucidate the molecular mechanisms underlying the N-glycan regulation of the invasive function of MMP-9 in gastric cancer biology.…”

Section: Expression Of Invasion-related Factors In the Bgc823/gnt-v Cmentioning

confidence: 99%

“…Furthermore, EGFR expression has also been shown to correlate with MMP expression in breast cancer cell lines and non-small cell lung cancer (15,26). MMPs are a family of zinc-containing endopeptidases, among which, MMP-2 and MMP-9 are highly expressed in aggressive tumors (27)(28)(29)(30). However, the precise mechanism of GnT-V regarding the association of EGFR signaling, EMT and MMPs in gastric cancer still remains largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Downregulation of the GnT-V gene inhibits metastasis and invasion of BGC823 gastric cancer cells

et al. 2013

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Abstract. Metastatic and invasive potential is a barrier to the successful treatment of gastric cancer. N-acetylglucosaminyltransferase V (GnT-V), a key enzyme catalyzing the formation of 1,6 N-acetylglucosamine (GlcNAc), has been demonstrated to display a distinct function in different types of tumors. The aim of this study was to investigate the role of GnT-V in the invasive potential of BGC823 human gastric cancer cells in vitro and the possible underlying mechanism. GnT-V was downregulated in BGC823 cells by oligo-siRNA transfection. Cell proliferation and invasiveness were assessed by CCK-8 assay, TUNEL assay, scratch-wound assay as well as Transwell assay. The products of GnT-V, β1-6 branching of asparagine-linked oligosaccharides, were determined by L-PHA lectin blot analysis. The expression of EGFRs, E-cadherin/vimentin and MMP-2/MMP-9 was analyzed both at the mRNA and protein levels. The results showed that downregulation of GnT-V decreased proliferation and the metastatic/invasive potential of BGC823 cells. The expression of EGFRs, E-cadherin/vimentin and MMP-9, molecules related to cancer metastasis and invasion in various tumors, were influenced correspondingly. These findings suggest that downregulation of GnT-V inhibited cell metastasis and invasion of BGC823 cells via EGFR signaling-initiated EMT phenotype and MMP-9 expression. These results provide a novel mechanism to explain the role of GnT-V in cell metastasis and invasion.

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Matrix metalloproteinase-2 and -9 in the sera and in the urine of human oncocytoma and renal cell carcinoma

Cited by 28 publications

References 21 publications

Matrix Metalloproteinases in Renal Diseases: A Critical Appraisal

Matrix Metalloproteinases in Renal Diseases: A Critical Appraisal

Epigenetic silencing of DACH1 induces the invasion and metastasis of gastric cancer by activating TGF‐β signalling

Downregulation of the GnT-V gene inhibits metastasis and invasion of BGC823 gastric cancer cells

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