Multiple uses of basement membrane‐like matrix (BME/Matrigel) <i>in vitro</i> and <i>in vivo</i> with cancer cells

Benton, Gabriel; Kleinman, Hynda K.; George, Jay; Arnaoutova, Irina

doi:10.1002/ijc.25781

Cited by 184 publications

(135 citation statements)

References 53 publications

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“…To facilitate analysis of small developing tumors at the earlier time points, tumor cells were injected in combination with Matrigel (22), which provides a support for tumor establishment. Interestingly, NK cells infiltrating RMA-S-derived tumors were anergic after only 7 days ( Figure 3E), suggesting that NK cell anergy induction occurred relatively early in tumor development.…”

Section: Resultsmentioning

confidence: 99%

Cytokine therapy reverses NK cell anergy in MHC-deficient tumors

Ardolino¹,

Azimi²,

Iannello³

et al. 2014

J. Clin. Invest.

159

169

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fit of the cytokine treatment in mice with RMA-S tumors was completely abrogated if the mice were NK-depleted, demonstrating that the effect of the cytokines depended on NK cells ( Figure 1C).The efficacy of cytokine treatments in mice bearing RMA-S tumors did not apply to mice bearing RMA tumors, which are similar to RMA-S cells except that they express high amounts of MHC class I and are therefore resistant to NK cells ( Figure 1B, bottom panel). The survival time in mice with RMA tumors did not change when the mice were treated with cytokines, and was similarly rapid to that in untreated mice with RMA-S tumors.Recently, Levin and colleagues described the "superkine" H9, an engineered version of IL-2, which functions independently of the α chain (CD25) of the IL-2 receptor. Compared with WT IL-2, H9 exhibits much more activity on NK cells and T cells. In vivo, H9 stimulated rejection of B16F10 melanoma tumors in B6 mice (13), but the role of NK cells in rejection has not been investigated. We tested whether H9 induces NK-dependent rejection of MHC class I-deficient tumors by implanting high doses of RMA-S or RMA cells and initiating H9 treatment after 7 days. Similar to the results with IL-12+IL-18 treatment, H9 resulted in improved survival of RMA-S-bearing mice, but had no effect in RMA-bearing mice (Figure 2, A and B). Notably, when mice were depleted of NK cells, the efficacy of H9 treatment was abolished (Figure 2A). These results show that H9 exerts its antitumor effect against MHC class I-deficient tumor cells in an NK cell-dependent fash-

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Section: Resultsmentioning

confidence: 99%

Cytokine therapy reverses NK cell anergy in MHC-deficient tumors

Ardolino¹,

Azimi²,

Iannello³

et al. 2014

J. Clin. Invest.

159

169

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“…MMP-14 enhances cell attachment to matrix, suggesting that MMP-14 can facilitate cell attachment at a new site for metastasis, aside from its leading role in matrix degradation (41). Matrigel, a solubilized basement membrane preparation extracted from EHS mouse sarcoma, resembles the biologically active matrix, and its major components include laminin, collagen IV, heparan sulfate proteoglycans, and entactin (42). In this study, we showed that miR-9 inhibited the MMP-14 expression and reduced the adhesion of neuroblastoma cells to Matrigel or fibronectin.…”

Section: Discussionmentioning

confidence: 99%

microRNA-9 Targets Matrix Metalloproteinase 14 to Inhibit Invasion, Metastasis, and Angiogenesis of Neuroblastoma Cells

Zhang

et al. 2012

Molecular Cancer Therapeutics

139

156

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Matrix metalloproteinase (MMP)-14 is the only membrane-anchored MMP that plays a critical role in tumor metastasis and angiogenesis. However, the mechanisms underlying MMP-14 expression in tumors still remain largely unknown. In this study, MMP-14 immunostaining was identified in 29/42 neuroblastoma tissues, which was correlated with clinicopathologic features and shorter patients' survival. In subtotal 20 neuroblastoma cases, microRNA 9 (miR-9) was downregulated and inversely correlated with MMP-14 expression. Bioinformatics analysis revealed a putative miR-9-binding site in the 3 0 -untranslated region (3 0 -UTR) of MMP-14 mRNA. Overexpression or knockdown of miR-9 responsively altered both the mRNA and protein levels of MMP-14 and its downstream gene, vascular endothelial growth factor, in cultured neuroblastoma cell lines SH-SY5Y and SK-N-SH. In an MMP-14 3 0 -UTR luciferase reporter system, miR-9 downregulated the luciferase activity, and these effects were abolished by a mutation in the putative miR-9-binding site. Overexpression of miR-9 suppressed the invasion, metastasis, and angiogenesis of SH-SY5Y and SK-N-SH cells in vitro and in vivo. In addition, the effects of miR-9 on MMP-14 expression, adhesion, migration, invasion, and angiogenesis were rescued by overexpression of MMP-14 in these cells. Furthermore, anti-miR-9 inhibitor or knockdown of MMP-14 respectively increased or inhibited the migration, invasion, and angiogenesis of neuroblastoma cells. These data indicate that miR-9 suppresses MMP-14 expression via the binding site in the 3 0 -UTR, thus inhibiting the invasion, metastasis, and angiogenesis of neuroblastoma.

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“…The 3D model of endothelial tubules (EC cultured alone on BME/Matrigel), is recognized as a reliable model of angiogenesis [25]. Notably EC exhibit a normal polarization [24].…”

Section: Discussionmentioning

confidence: 99%

Pilot Study on “Pericytic Mimicry” and Potential Embryonic/Stem Cell Properties of Angiotropic Melanoma Cells Interacting with the Abluminal Vascular Surface

Lugassy

Wadehra

et al. 2012

Cancer Microenvironment

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The interaction of tumor cells with the tumor vasculature is mainly studied for its role in tumor angiogenesis and intravascular metastasis of circulating tumor cells. In addition, a specific interaction of tumor cells with the abluminal surfaces of vessels, or angiotropism, may promote the migration of angiotropic tumor cells along the abluminal vascular surfaces in a pericytic location. This process has been termed extravascular migratory metastasis.The abluminal vascular surface may also provide a vascular niche inducing or sustaining stemness to angiotropic tumor cells. This pilot study investigated if angiotropic melanoma cells might represent a subset population with pericytic and embryonic or stem cell properties. Through microarray analysis, we showed that the interaction between melanoma cells and the abluminal surface of endothelial cells triggers significant differential expression of several genes. The most significantly differentially expressed genes have demonstrated properties linked to cancer cell migration (CCL2, ICAM1 and IL6), cancer progression (CCL2, ICAM1, SELE, TRAF1, IL6, SERPINB2 and CXCL6), epithelial to mesenchymal transition (CCL2 and IL6), embryonic/stem cell properties (CCL2, PDGFB, EVX1 and CFDP1) and pericytic recruitment (PDGFB). In addition, bioinformatics-based analysis of the differentially expressed genes has shown that the most significantly enriched functional groups included development, cell movement, cancer, and embryonic development. Finally, the investigation of pericyte/mesenchymal stem cells markers via immunostaining of human melanoma samples revealed expression of PDGFRB, NG2 and CD146 by angiotropic melanoma cells. Taken together, these preliminary data are supportive of the "pericytic mimicry" by angiotropic melanoma cells, and suggest that the interaction between melanoma cells and the abluminal vascular surface induce differential expression of genes linked to cancer migration and embryonic/ stem cell properties.

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Multiple uses of basement membrane‐like matrix (BME/Matrigel) in vitro and in vivo with cancer cells

Cited by 184 publications

References 53 publications

Cytokine therapy reverses NK cell anergy in MHC-deficient tumors

Cytokine therapy reverses NK cell anergy in MHC-deficient tumors

microRNA-9 Targets Matrix Metalloproteinase 14 to Inhibit Invasion, Metastasis, and Angiogenesis of Neuroblastoma Cells

Pilot Study on “Pericytic Mimicry” and Potential Embryonic/Stem Cell Properties of Angiotropic Melanoma Cells Interacting with the Abluminal Vascular Surface

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