Expression of matrix metalloproteinase 9 is a prognostic factor in patients with non‐Hodgkin lymphoma

Sakata, Koh‐ichi; Satoh, Masaaki; Someya, Masanori; Asanuma, Chie; Nagakura, Hisayasu; Oouchi, Atsushi; Nakata, Kensei; Kogawa, Katsuhisa; Koito, Kazumitsu; Hareyama, Masato; Himi, Tetsuo

doi:10.1002/cncr.11905

Cited by 62 publications

(57 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…MMP9 is also critical for B-CLL invasion and progression and has been defined as a prognostic factor in patients with nonHodgkin's lymphoma (Sakata et al, 2004;RedondoMunoz et al, 2006). The transcriptional induction of MMP9 is regulated by NF-kB in HTLV-I-or in Epstein-Barr virus-infected cells (Yoshizaki et al, 1998;Mori et al, 2002) as well as on TNFa stimulation in skeletal muscle cells (Srivastava et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Matrix Metalloproteinase-9 gene induction by a truncated oncogenic NF-κB2 protein involves the recruitment of MLL1 and MLL2 H3K4 histone methyltransferase complexes

et al. 2009

View full text Add to dashboard Cite

Constitutive nuclear factor (NF)-jB activation in haematological malignancies is caused in several cases by loss of function mutations within the coding sequence of NF-jB inhibitory molecules such as IjBa or p100. Hut-78, a truncated form of p100, constitutively generates p52 and contributes to the development of T-cell lymphomas but the molecular mechanism underlying this oncogenic potential remains unclear. We show here that MMP9 gene expression is induced through the alternative NF-jB-activating pathway in fibroblasts and also on Hut-78 or p52 overexpression in fibroblasts as well as in lymphoma cells. p52 is critical for Hut-78-mediated MMP9 gene induction as a Hut-78 mutant as well as other truncated NF-jB2 proteins that are not processed into p52 failed to induce the expression of this metalloproteinase. Conversely, MMP9 gene expression is impaired in p52-depleted HUT-78 cells. Interestingly, MLL1 and MLL2 H3K4 methyltransferase complexes are tethered by p52 on the MMP9 but not on the IjBa promoter, and the H3K4 trimethyltransferase activity recruited on the MMP9 promoter is impaired in p52-depleted HUT-78 cells. Moreover, MLL1 and MLL2 are associated with Hut-78 in a native chromatin-enriched extract. Thus, we identified a molecular mechanism by which the recruitment of a H3K4 histone methyltransferase complex on the promoter of a NF-jB-dependent gene induces its expression and potentially the invasive potential of lymphoma cells harbouring constitutive activity of the alternative NF-jB-activating pathway.

show abstract

Section: Introductionmentioning

confidence: 99%

Matrix Metalloproteinase-9 gene induction by a truncated oncogenic NF-κB2 protein involves the recruitment of MLL1 and MLL2 H3K4 histone methyltransferase complexes

et al. 2009

View full text Add to dashboard Cite

show abstract

“…4) have been described in the metastatic process. For example, elevated expression of MMP-9 correlates with a poor clinical outcome in patients within non-Hodgkin's lymphoma (5,6).…”

Section: Introductionmentioning

confidence: 99%

A Novel Function for Galectin-7: Promoting Tumorigenesis by Up-regulatingMMP-9Gene Expression

2005

View full text Add to dashboard Cite

Metastasis is a multistep process by which cancer cells, after acquiring several capabilities, spread to distinct sites in the body. It is the major cause of death in individuals suffering from cancer. We have recently identified galectin-7 as a new gene associated with the progression of T cell lymphoma toward a metastatic phenotype, suggesting a possible causal relationship. The present study was designed to investigate the role of galectin-7 in lymphoma. We found that the development of thymic lymphoma was accelerated when induced by lymphoma cells overexpressing galectin-7. Moreover, transfection of an expression vector containing the galectin-7 gene in low metastatic lymphoma cells increased their metastatic behavior and confers these cells with the new ability to overcome the resistance of intercellular adhesion molecule-1-deficient mice to lymphoma dissemination. Finally, we provide data suggesting that galectin-7 modulates the aggressive behavior of lymphoma cells by controlling the expression of metastatic genes, such as MMP-9. This hypothesis is based on the following evidence: (a) galectin-7 transfectants have higher levels of MMP-9 expression, (b) addition of B-lactose completely inhibits expression of MMP-9 by galectin-7 transfectants, and (c) recombinant forms of galectin-7 induces the expression of MMP-9 in both mouse and human lymphoma cells. Our results have uncovered the existence of a previously undescribed activity, the promotion of cancer cell malignancy, to galectin-7. (Cancer Res 2005; 65(12): 5205-10)

show abstract

“…These include genes codifying for matrix metallopeptidases and their inhibitors, cathepsins and chemokines, among others [114][115][116][117][118][119][120][121][122][123][124][125][126][127][128][129].…”

Section: Cell Motility and Tissue Invasionmentioning

confidence: 99%

“…Proteolytic enzymes: Tumor invasion and metastasis are facilitated by the up-regulation of various types of proteases, which induce the escape of cancer cells from the primary site, by breaking down the connective tissue and basement membrane, such as metalloproteinases and cathepsins both of which appear to be affected in NKTCL [114][115][116][117][118][119][120][121][122][123][124].…”

Section: Cell Motility and Tissue Invasionmentioning

confidence: 99%

“…The activity of MMP is inhibited by tissue inhibitors of metalloproteases (TIM, 1 to 4) [117]. The unbalance of the expression of MMP and TIMP may contribute to the extensive necrosis observed in NKTCL, as well as to the tendency of these tumors to disseminate locally [120][121][122][123]. For instance, on a study in which the expression of MMP-1, -2, -3, -9, -11, -13 and TIMP-1 and -2 was evaluated by immunohistochemistry revealed that NKTCL cells and fibroblasts were positive for MMP-1 and MMP-11 in most of the cases, whereas MMP-2, -3 and -9 were expressed in neoplastic cell in between 30 to 65% of the cases; TIMP-1 was presented mainly in the epithelium and TIMP-2 was poor expressed of the all cases [120].…”

Section: Cell Motility and Tissue Invasionmentioning

confidence: 99%

See 1 more Smart Citation

Aggressive Mature Natural Killer Cell Neoplasms: from Disease Biology to Disease Manifestations

2014

J Blood Disord Transfus 2014

View full text Add to dashboard Cite

Expression of matrix metalloproteinase 9 is a prognostic factor in patients with non‐Hodgkin lymphoma

Cited by 62 publications

References 30 publications

Matrix Metalloproteinase-9 gene induction by a truncated oncogenic NF-κB2 protein involves the recruitment of MLL1 and MLL2 H3K4 histone methyltransferase complexes

Matrix Metalloproteinase-9 gene induction by a truncated oncogenic NF-κB2 protein involves the recruitment of MLL1 and MLL2 H3K4 histone methyltransferase complexes

A Novel Function for Galectin-7: Promoting Tumorigenesis by Up-regulatingMMP-9Gene Expression

Aggressive Mature Natural Killer Cell Neoplasms: from Disease Biology to Disease Manifestations

Contact Info

Product

Resources

About