Critical role for matrix metalloproteinase‐9 in platelet‐activating factor‐induced experimental tumor metastasis

Ko, Hyun-Mi; Kang, Ji-Hyoun; Jung, Bongnam; Kim, Han-A; Park, Sung Jun; Kim, Kyoung-Jin; Kang, Yeong-Rim; Lee, Hern-Ku; Im, Suhn-Young

doi:10.1002/ijc.22450

Cited by 18 publications

(18 citation statements)

References 39 publications

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“…MMP-2 and MMP-9 overexpression by pulmonary cells is able to increment the number of lung metastasis in experimental models [54,57]. The increased expression of MMP-9, but not MMP-2, in the lung significantly enhanced the pulmonary metastasis of murine melanoma cells B16F10 [95]. In agreement with this finding the inhibition of the expression of MMP-2 and MMP-9 in the mouse lung reduced lung metastases from B16F10 [96].…”

Section: Lung Metastasissupporting

confidence: 84%

Roles of Metalloproteases in Metastatic Niche

Rucci

Sanità²,

Angelucci

2011

CMM

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Metalloproteinases (MMPs) are a cluster of at least 23 enzymes belonging to the more wide family of endopeptidases called Metzincins, whose structure is characterized by the presence of a zinc ion at the catalytic site. Although the general view of MMPs as physiologic scissors involved in extracellular matrix (ECM) degradation and tissue remodeling is still valid, additional functions have recently emerged, including the ability to cleave non ECM molecules such as growth factors, cytokines and chemokines from their membrane-anchored proforms. These functions are utilized by tumor cells and are fundamental in the determination of tumor progression and invasion. The effect of MMPs activity in cancer progression has been traditionally associated with the acquisition by tumor cells of an invasive phenotype, an indispensable requisite for the metastatic spreading of cancer cells. In addition to the traditional view, a new role for MMPs in creating a favourable microenvironment has been proposed, so that MMPs are not only involved in cell invasion, but also in signaling pathways that control cell growth, inflammation, or angiogenesis. Finally, recent evidence suggest a role of MMPs in the so called "pre-metastatic niche" that is the hypothesis of an early distant modification of the premetastatic site by primary cancer cells. This new hypothesis is changing our traditional view about MMPs and provides important insights into the effective time window for the therapeutic use of MMP inhibitors. In this review we provide the main available data about the ability of MMPs in creating a suitable microenvironment for tumor growth in metastatic sites and we indicate the implication of these data on the potential use of MMP inhibitors in the metastatic therapy.

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Section: Lung Metastasissupporting

confidence: 84%

Roles of Metalloproteases in Metastatic Niche

Rucci

Sanità²,

Angelucci

2011

CMM

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“…This is promising because cathepsins have been shown to increase metastatic potential by facilitating cell migration and invasiveness. The antineoplastic activity of bryostatin-1 has previously been reported in a number of murine and human tumors and cell lines, including breast, lung, and lymphoma [22–23,59]. Thus, our study suggests that the simultaneous induction of immune components in melanoma cells while restricting tumor growth and invasion by bryostatin-1, may contribute to the design of successful chemo-immunotherapeutics against metastatic melanoma.…”

Section: Discussionsupporting

confidence: 70%

Enhancement of HLA class II-restricted CD4+ T cell recognition of human melanoma cells following treatment with bryostatin-1

Zhao¹,

Amria²,

Hossain³

et al. 2011

Cellular Immunology

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The majority of melanoma cells express detectable levels of HLA class II proteins, and an increased threshold of cell surface class II is crucial for the stimulation of CD4+ T cells. Bryostatin-1, a protein kinase C (PKC) activator, has been considered as a potent chemotherapeutic agent in a variety of in vitro tumor models. Little is known about the role of bryostatin-1 in HLA class II Ag presentation and immune activation in malignant tumors, especially in melanoma. In this study, we show that bryostatin-1 treatment enhances CD4+ T cell recognition of melanoma cells in the context of HLA class II molecules. We also show that bryostatin-1 treatment of melanoma cells increases class II protein levels by upregulating the class II transactivator (CIITA) gene. Flow cytometry and confocal microscopic analyses revealed that bryostatin-1 treatment upregulated the expression of costimulatory molecules (CD80 and CD86) in melanoma cells, which could prolong the interaction of immune cells and tumors. Bryostatin-1 also induced cellular differentiation in melanoma cells, and reduced tumorigenic factors such as pro-cathepsins and matrix-metalloproteinase-9. These data suggest that bryostatin-1 could be used as a chemo-immunotherapeutic agent for reducing tumorigenic potential of melanoma cells while enhancing CD4+ T cell recognition to prevent tumor recurrence.

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“…Most recently, Fallani et al have demonstrated that PAF is being synthesized by B16F10 cells in response to INF-γ treatment, and that PAF promoted the invasion of these cells through the Matrigel-coated filters [110]. Moreover, it has been shown that a single intraperitoneal injection of PAF induced expression of MMP-9 and MMP-2 in the mouse lungs, and significantly enhanced B16F10 pulmonary lung metastasis, suggesting an addition, non-tumor-cell mechanism of PAF action [111]. Finally, in the human melanoma cell line Hs294T, PAFR antagonists were able to prevent adhesion to IL-1-stimulated endothelial cells [112].…”

Section: Paf and Paf Receptor In Melanomamentioning

confidence: 95%

Inflammation and melanoma growth and metastasis: The role of platelet-activating factor (PAF) and its receptor

Melnikova

Bar‐Eli

2007

Cancer Metastasis Rev

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An inflammatory tumor microenvironment fosters tumor growth, angiogenesis and metastatic progression. Platelet-activating factor (PAF) is an inflammatory biolipid produced from membrane glycerophospholipids. Through the activity of its G-protein coupled receptor, PAF triggers a variety of pathological reactions including tumor neo-angiogenesis. Several groups have demonstrated that inhibiting PAF-PAF receptor pathway at the level of a ligand or receptor results in an effective inhibition of experimental tumor growth and metastasis. In particular, our group has recently demonstrated that PAF receptor antagonists can effectively inhibit the metastatic potential of human melanoma cells in nude mice. Furthermore, we showed that PAF stimulated the phosphorylation of CREB and ATF-1 in metastatic melanoma cells, which resulted in overexpression of MMP-2 and MT1-MMP. Our data indicate that PAF acts as a promoter of melanoma metastasis in vivo. Since only metastatic melanoma cells overexpress CREB/ATF-1, we propose that these cells are better equipped to respond to PAF within the tumor microenvironment when compared to their non-metastatic counterparts.

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Critical role for matrix metalloproteinase‐9 in platelet‐activating factor‐induced experimental tumor metastasis

Cited by 18 publications

References 39 publications

Roles of Metalloproteases in Metastatic Niche

Roles of Metalloproteases in Metastatic Niche

Enhancement of HLA class II-restricted CD4+ T cell recognition of human melanoma cells following treatment with bryostatin-1

Inflammation and melanoma growth and metastasis: The role of platelet-activating factor (PAF) and its receptor

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