Fibronectin and sialic acid levels in human meningiomas and gliomas

Sönmez, Hüseyin; Kökoğlu, Emine; Süer, Selma; Özyurt, Emin

doi:10.1016/0304-3835(95)03692-p

Cited by 6 publications

(6 citation statements)

References 26 publications

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“…One clear‐cut explanation to account for the widespread transduction profile of the various AAV serotypes is that the different AAV receptors are widely expressed by glioma cells. This contention is supported by previous experiments showing that the attachment molecules for AAV2, AAV4 or AAV5 are expressed in human glioblastoma cells and biopsy specimens 37, 46. These observations may have important implications for future therapeutic interventions.…”

Section: Discussionsupporting

confidence: 56%

Adeno‐associated virus (AAV) serotypes 2, 4 and 5 display similar transduction profiles and penetrate solid tumor tissue in models of human glioma

Thorsen

Afione

Huszthy

et al. 2006

The Journal of Gene Medicine

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Section: Discussionsupporting

confidence: 56%

Adeno‐associated virus (AAV) serotypes 2, 4 and 5 display similar transduction profiles and penetrate solid tumor tissue in models of human glioma

Thorsen

Afione

Huszthy

et al. 2006

The Journal of Gene Medicine

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“…Fibronectin and laminin are two components of brain extracellular matrix that have been found to be upregulated in glioblastoma, and both may play a role in tumor migration and invasion [17, 19]. Evidence suggests that differential interaction with matrix components may affect the migrational and proliferative capabilities of tumor cell lines.…”

Section: Resultsmentioning

confidence: 99%

“…Many structural matrix components are overexpressed or mutated in GBM, and tumor cells may in fact express components that can increase their migratory capabilities [17, 19]. The fibronectin 1 ( FN1 ) gene carried a mutation in 1 tumor, and the COL3A1 gene was considered a potential driver by Parsons et al, with 3 mutations in individual tumors [6].…”

Section: Discussionmentioning

confidence: 99%

“…Cell attachments, along with receptor and focal adhesion turnover and cytoskeleton changes, are controlled in part by complex interactions between integrins, receptor tyrosine kinases, and pathways such as focal adhesion kinase (FAK) and phosphatidylinositol 3-kinase (PI3K) signaling [12-16]. Several ECM components themselves, including laminin and fibronectin, have been shown to be overexpressed in tumors, and downregulation of these components reduces invasion and migration of glioblastoma cells [17-21]. The rate of proliferation of invading tumor cells is often significantly decreased when compared to cells in the main tumor mass [8, 9].…”

Section: Introductionmentioning

confidence: 99%

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Abrogation of PIK3CA or PIK3R1 reduces proliferation, migration, and invasion in glioblastoma multiforme cells

et al. 2011

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Glioblastoma multiforme (GBM) is a highly invasive and deadly brain tumor. Tumor cell invasion makes complete surgical resection impossible and reduces the efficacy of other therapies. Genome-wide analyses of mutations, copy-number changes, and expression patterns have provided new insights into genetic abnormalities common in GBM. We analyzed published data and identified the invasion and motility pathways most frequently altered in GBM. These were most notably the focal adhesion and integrin signaling, and extracellular matrix interactions pathways. We mapped alterations in each of these pathways and found that they included the catalytic PIK3CA and regulatory PIK3R1 subunit genes of the class IA PI3K. Knockdown of either of these genes separately in GBM cell lines by lentiviral-mediated shRNA expression resulted in decreased proliferation, migration, and invasion in all lines tested. FAK activity was reduced by knockdown of either PIK3CA or PIK3R1, and MMP2 levels were reduced by knockdown of PIK3R1. We conclude that PIK3R1, like PIK3CA, is a potential therapeutic target in GBM and that it also influences tumor cell growth and motility.

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“…First, AAVs are packaged into significantly smaller capsids compared to other viral vectors. Second, the receptor molecules for several AAV serotypes appear widely expressed in tumor tissue (Isaka et al, 1994;Sonmez et al, 1995;Shee et al, 1998;…”

Section: Discussionmentioning

confidence: 99%

Widespread Dispersion of Adeno-Associated Virus Serotype 1 and Adeno-Associated Virus Serotype 6 Vectors in the Rat Central Nervous System and in Human Glioblastoma Multiforme Xenografts

Huszthy

Svendsen²,

Wilson³

et al. 2005

Human Gene Therapy

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The transduction patterns of recombinant adeno-associated virus serotype 1 (AAV1) and serotype 6 (AAV6) vectors were assessed in human glioblastoma multiforme (GBM) cell lines, in human GBM biopsy spheroids, and in tumor xenografts growing in nude rat brains. All the cell lines tested (A172, D37, GaMg, HF66, and U373Mg) were found to be permissive to both AAV1 and AAV6 vectors, and thus displayed a transduction pattern similar to AAV2 vectors. For every cell line tested, the transduction efficiency displayed by AAV2 vectors was better than by isogenic and isopromoter AAV1 vectors. Transduction efficiency was dependent on the viral particle number used, suggesting that the receptors for these vectors are widely distributed in GBM tissues. Interestingly, AAV1, AAV2, and AAV6 vectors were able to infect and transduce the same cells when added simultaneously to monolayer cultures. Infection of human GBM biopsy spheroids with AAV1 and AAV6 vectors resulted in transgene expression both at the surface layers and in the core of the spheroids. Following injection of AAV1 and AAV6 vectors into human GBM biopsy xenografts growing in nude rat brains, reporter gene expression was seen both in the periphery as well as in the central regions of the tumors. When injected into the normal rat brain, both AAV1 and AAV6 vectors were found to transduce several central nervous system (CNS) regions. The presented results suggest a potential therapeutic role for AAV1 and AAV6 vectors in gene therapy for GBM and also for other CNS malignancies.

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Fibronectin and sialic acid levels in human meningiomas and gliomas

Cited by 6 publications

References 26 publications

Adeno‐associated virus (AAV) serotypes 2, 4 and 5 display similar transduction profiles and penetrate solid tumor tissue in models of human glioma

Adeno‐associated virus (AAV) serotypes 2, 4 and 5 display similar transduction profiles and penetrate solid tumor tissue in models of human glioma

Abrogation of PIK3CA or PIK3R1 reduces proliferation, migration, and invasion in glioblastoma multiforme cells

Widespread Dispersion of Adeno-Associated Virus Serotype 1 and Adeno-Associated Virus Serotype 6 Vectors in the Rat Central Nervous System and in Human Glioblastoma Multiforme Xenografts

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