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Norman, Sylvia A.; Golfinos, John G.; Scheck, Adrienne C.

doi:10.1023/a:1005840420136

Cited by 16 publications

(7 citation statements)

References 26 publications

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“…According to previous descriptions and as shown for each set schematically, these primer pairs bind to specific regions of the three RPTPβ/ζ isoforms ( Figure 2 A; [ 45 ]). The glioblastoma multiforme cell line U-251 served as positive control, since all RPTPβ/ζ isoforms are prominently expressed in different grades of glioma types [ 45 ].…”

Section: Resultsmentioning

confidence: 99%

“…By combining different primer pairs, modified according to Norman et al, unique RPTPβ/ζ (PTPRZ1) isoforms were analyzed via semi-quantitative RT-PCR ( Table 2 ) [ 45 ]. RT-PCR using CP and EC primer pairs was performed with Taq DNA Polymerase (Sigma-Aldrich).…”

Section: Methodsmentioning

confidence: 99%

“…Abbreviations: bp-base pairs, for-forward, rev-reverse. [45]. RT-PCR using CP and EC primer pairs was performed with Taq DNA Polymerase (Sigma-Aldrich).…”

Section: Quantitative Real-time Pcr Analyses (Rt-qpcr)mentioning

confidence: 99%

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Expression Changes and Impact of the Extracellular Matrix on Etoposide Resistant Human Retinoblastoma Cell Lines

Reinhard

Wagner

Krämer

et al. 2020

IJMS

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Retinoblastoma (RB) represents the most common malignant childhood eye tumor worldwide. Several studies indicate that the extracellular matrix (ECM) plays a crucial role in tumor growth and metastasis. Moreover, recent studies indicate that the ECM composition might influence the development of resistance to chemotherapy drugs. The objective of this study was to evaluate possible expression differences in the ECM compartment of the parental human cell lines WERI-RB1 (retinoblastoma 1) and Y79 and their Etoposide resistant subclones via polymerase chain reaction (PCR). Western blot analyses were performed to analyze protein levels. To explore the influence of ECM molecules on RB cell proliferation, death, and cluster formation, WERI-RB1 and resistant WERI-ETOR cells were cultivated on Fibronectin, Laminin, Tenascin-C, and Collagen IV and analyzed via time-lapse video microscopy as well as immunocytochemistry. We revealed a significantly reduced mRNA expression of the proteoglycans Brevican, Neurocan, and Versican in resistant WERI-ETOR compared to sensitive WERI-RB1 cells. Also, for the glycoproteins α1-Laminin, Fibronectin, Tenascin-C, and Tenascin-R as well as Collagen IV, reduced expression levels were observed in WERI-ETOR. Furthermore, a downregulation was detected for the matrix metalloproteinases MMP2, MMP7, MMP9, the tissue-inhibitor of metalloproteinase TIMP2, the Integrin receptor subunits ITGA4, ITGA5 and ITGB1, and all receptor protein tyrosine phosphatase β/ζ isoforms. Downregulation of Brevican, Collagen IV, Tenascin-R, MMP2, TIMP2, and ITGA5 was also verified in Etoposide resistant Y79 cells compared to sensitive ones. Protein levels of Tenascin-C and MMP-2 were comparable in both WERI cell lines. Interestingly, Fibronectin displayed an apoptosis-inducing effect on WERI-RB1 cells, whereas an anti-apoptotic influence was observed for Tenascin-C. Conversely, proliferation of WERI-ETOR cells was enhanced on Tenascin-C, while an anti-proliferative effect was observed on Fibronectin. In WERI-ETOR, cluster formation was decreased on the substrates Collagen IV, Fibronectin, and Tenascin-C. Collectively, we noted a different ECM mRNA expression and behavior of Etoposide resistant compared to sensitive RB cells. These findings may indicate a key role of ECM components in chemotherapy resistance formation of RB.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Expression Changes and Impact of the Extracellular Matrix on Etoposide Resistant Human Retinoblastoma Cell Lines

Reinhard

Wagner

Krämer

et al. 2020

IJMS

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“…Motile glioma cells can remodel this matrix by local degradation of ECM molecules and synthesis of a novel pericellular scaffold (11). The glioma ECM contains molecules that predominate during neural development (hyaluronic acid, phosphacan, SPARC) (14, 15), mesenchymal proteins found in peripheral stroma and basal lamina (collagens, fibronectin) (16), and chondroitin sulfate proteoglycans that limit cell motility in the adult CNS (versican, brevican) (17, 18) but instead promote glioma cell migration (7, 19, 20). Recent evidence from our and other laboratories has suggested that the presence of both mesenchymal and neural-specific matrix proteins in gliomas may result in novel molecular interactions that specifically promote glioma cell motility in the CNS (19, 21).…”

mentioning

confidence: 99%

Fibulin-3 Is Uniquely Upregulated in Malignant Gliomas and Promotes Tumor Cell Motility and Invasion

Rajamani

Sim

et al. 2009

Molecular Cancer Research

118

161

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Malignant gliomas are highly invasive tumors with an almost invariably rapid and lethal outcome. Surgery and chemoradiotherapy fail to remove resistant tumor cells that disperse within normal tissue, which are a major cause for disease progression and therapy failure. Infiltration of the neural parenchyma is a distinctive property of malignant gliomas compared to other solid tumors. Thus, glioma cells are thought to produce unique molecular changes that remodel the neural extracellular matrix and form a microenvironment permissive for their motility. Here we describe the unique expression and pro-invasive role of fibulin-3, a mesenchymal matrix protein specifically upregulated in gliomas. Fibulin-3 is downregulated in peripheral tumors and thought to inhibit tumor growth. However, we found fibulin-3 highly upregulated in gliomas and cultured glioma cells, although the protein was undetectable in normal brain or cultured astrocytes. Overexpression and knockdown experiments revealed that fibulin-3 did not seem to affect glioma cell morphology or proliferation, but enhanced substrate-specific cell adhesion and promoted cell motility and dispersion in organotypic cultures. Moreover, orthotopic implantation of fibulin-3-overexpressing glioma cells resulted in diffuse tumors with increased volume and rostrocaudal extension compared to controls. Tumors and cultured cells overexpressing fibulin-3 also showed elevated expression and activity of matrix metalloproteases, such as MMP-2/9 and ADAMTS-5. Taken together, our results suggest that fibulin-3 has a unique expression and pro-tumoral role in gliomas, and could be a potential target against tumor progression. Strategies against this glioma-specific matrix component could disrupt invasive mechanisms and restrict dissemination of these tumors.

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“…Among these genes we find several known to be associated with cancers. PTPRT , a protein tyrosine phosphatase receptor, is a signaling molecule known to be implicated in oncogenic transformation in several different cancers 13 , including colon cancer 14,15 , glioma 16 , and melanoma 17 . NELL1 and NELL2 , growth factor like protein thought to be involved in regulation of cell growth, has also been associated with multiple cancer types, including esophageal adenocarcinoma 18 , colon cancer and Burkitt’s lymphoma 19 .…”

Section: Discussionmentioning

confidence: 99%

Matching Cancer Genomes to Established Cell Lines for Personalized Oncology

Dudley¹,

Chen²,

Butte³

2010

Biocomputing 2011

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The diagnosis and treatment of cancers, which rank among the leading causes of mortality in developed nations, presents substantial clinical challenges. The genetic and epigenetic heterogeneity of tumors can lead to differential response to therapy and gross disparities in patient outcomes, even for tumors originating from similar tissues. High-throughput DNA sequencing technologies hold promise to improve the diagnosis and treatment of cancers through efficient and economical profiling of complete tumor genomes, paving the way for approaches to personalized oncology that consider the unique genetic composition of the patient's tumor. Here we present a novel method to leverage the information provided by cancer genome sequencing to match an individual tumor genome with commercial cell lines, which might be leveraged as clinical surrogates to inform prognosis or therapeutic strategy. We evaluate the method using a published lung cancer genome and genetic profiles of commercial cancer cell lines. The results support the general plausibility of this matching approach, thereby offering a first step in translational bioinformatics approaches to personalized oncology using established cancer cell lines.

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Untitled

Cited by 16 publications

References 26 publications

Expression Changes and Impact of the Extracellular Matrix on Etoposide Resistant Human Retinoblastoma Cell Lines

Expression Changes and Impact of the Extracellular Matrix on Etoposide Resistant Human Retinoblastoma Cell Lines

Fibulin-3 Is Uniquely Upregulated in Malignant Gliomas and Promotes Tumor Cell Motility and Invasion

Matching Cancer Genomes to Established Cell Lines for Personalized Oncology

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