Inhibition of adenovirus-mediated human MAGE-D1 on angiogenesis in vitro and in vivo

Shen, Weishou; Xue, Qiang; Zhu, Jun; Hu, Ben-Shun; Wu, Yi-Ding; Su, Qing

doi:10.1007/s11010-006-9373-6

Cited by 13 publications

(15 citation statements)

References 44 publications

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“…However, it must be emphasized that other MAGE A genes members, such as MAGE A4, have been reported to promote apoptosis in non-small cell lung cancer (39). In addition, MAGE D1 may represent a novel endogenous inhibitor of angiogenesis in vitro and in vivo (40). These pleiotropic functions highlight the importance of detailed MAGE characterization to better understand the putative actions of the various family members in cancer progression.…”

Section: Discussionmentioning

confidence: 99%

The Melanoma-Associated Antigen A3 Mediates Fibronectin-Controlled Cancer Progression and Metastasis

Liu¹,

Cheng²,

Sylvia³

et al. 2008

Cancer Research

121

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Tumor cells frequently exhibit decreased adhesiveness due to failure to deposit stromal fibronectin (FN), permitting more rapid proliferation, migration, invasion, and metastasis. Although up-regulation of FN has been noted in gene profiles of carcinomas compared with normal tissue, reduced FN expression has been described at the peripheral margins of invading tumors. In this study, we investigate the role of FN in cancer behavior. Using human thyroid carcinoma cells with stably down-regulated FN, we performed gene profiling and created an orthotopic mouse model. We stably overexpressed the FN target, MAGE A3, which has also been identified as a target of the breast cancer risk factor fibroblast growth factor receptor 2, and examined the functional effects in vitro and in vivo in a flank model and an orthotopic model of thyroid cancer. Mouse xenografts showed significantly enhanced tumor growth as well as larger and more numerous lung metastases in response to FN silencing. Gene profiling identified the melanoma-associated antigen (MAGE A3) as significantly up-regulated in response to FN silencing. Forced expression of MAGE A3 resulted in p21 down-regulation, accelerated cell cycle progression, increased cell migration rate, and invasion in vitro and in vivo in an orthotopic mouse model where microcomputed tomography confirmed lung metastases that recapitulate the progression of human thyroid cancer. We conclude that MAGE A3 is a functional integrator of diverse signals, including FGFR2 and FN, to modulate cancer progression.

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Section: Discussionmentioning

confidence: 99%

The Melanoma-Associated Antigen A3 Mediates Fibronectin-Controlled Cancer Progression and Metastasis

Liu¹,

Cheng²,

Sylvia³

et al. 2008

Cancer Research

121

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“…Overexpression of MAGE-D1 inhibits EC migration and adhesion, and disrupts cytoskeletal rearrangements and lamellipodia formation. 55 Not surprisingly, some classical axon guidance molecules also regulate tip cell navigation. The Netrin guidance receptor Unc5B is also expressed by endothelial tip cells.…”

Section: Novel Regulators Of Tip Cell Formationmentioning

confidence: 99%

Mechanisms of Vessel Branching

Smet

Segura

Bock

et al. 2009

ATVB

334

248

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Abstract-Filopodia, "the fingers that do the walking," have been identified on endothelial cells at the tip of sprouting vessels for half a century, but the key role of the tip cell in vessel branching has been recognized only in the past few years. A model is emerging, whereby tip cells lead the way in a branching vessel, stalk cells elongate the sprout, and a very recently discovered phalanx cell ensures quiescence and perfusion of the newly formed branch. Recent genetic studies have shed light on the molecular signature of these distinct endothelial phenotypes; this provides a novel conceptual framework of how vessel morphogenesis occurs. Here, we will discuss the molecular candidates that participate in the decision of endothelial cells to adapt these distinct fates and highlight the emerging insights on how these cells send out filopodia while navigating.

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“…Existing reports about the role of MAGED1 as an inhibitor of angiogenesis in endothelial cells, 20 incited us to explore the effects of Dlxin-1 as an anti-angiogenic protein in the glioma stem cells. For this, we focused on studying the effects of Dlxin-1 on brain colonization and vascularization in murine orthotopic xenografts generated by individually injecting about 1000 cells of HNGC-2-EV and HNGC-2-Dlxin intracranially in NOD-SCID mice.…”

Section: Suppression Of Tumorigenicity With Dlxin-1mentioning

confidence: 99%

Dlxin-1, a member of MAGE family, inhibits cell proliferation, invasion and tumorigenicity of glioma stem cells

et al. 2010

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We have previously reported the presence of Dlxin-1, a member of the melanoma antigen gene (MAGE) family, in the brain and showed its function as a cell cycle arrest protein, suggesting that Dlxin-1 may have anti-proliferative functions in rapidly growing tumors. Using the cancer stem cell hypothesis, which attributes the initiation and progression of brain tumors to the cancerinitiating stem cells, we have investigated the role of Dlxin-1 in the glioma stem cells propagated by us as a cell culture system comprising of HNGC-2 cells. Our studies provide evidence about the role of Dlxin-1 as an anti-tumorigenic protein in the highly chemo-resistant glioma stem cells. Next, we show that these anti-proliferative effects are manifested by Dlxin-1 through down regulation of the activities of MMP-2 and MMP-9, and through interaction of Dlxin-1 with its target protein P311 that is involved in glioma cell invasion. In summary, we establish the roles for Dlxin-1, one as an anti-tumorigenic and anti-invasive protein in highgrade gliomas and the other as an inducer of differentiation of glioma stem cells. These two attributes, in conjunction, result in conversion of the drug-resistant brain tumor stem cells to the tumor-attenuated cells that may now be more amenable to effective therapeutic targeting.

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Inhibition of adenovirus-mediated human MAGE-D1 on angiogenesis in vitro and in vivo

Cited by 13 publications

References 44 publications

The Melanoma-Associated Antigen A3 Mediates Fibronectin-Controlled Cancer Progression and Metastasis

The Melanoma-Associated Antigen A3 Mediates Fibronectin-Controlled Cancer Progression and Metastasis

Mechanisms of Vessel Branching

Dlxin-1, a member of MAGE family, inhibits cell proliferation, invasion and tumorigenicity of glioma stem cells

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