Search

Your search keyword '"Verbovšek, Urška"' showing total 10 results
Start Over Author "Verbovšek, Urška" Search Limiters Full Text
10 results on '"Verbovšek, Urška"'

1. Cathepsin K cleavage of SDF-1α inhibits its chemotactic activity towards glioblastoma stem-like cells

Author

Hira, Vashendriya V.V., primary, Verbovšek, Urška, additional, Breznik, Barbara, additional, Srdič, Matic, additional, Novinec, Marko, additional, Kakar, Hala, additional, Wormer, Jill, additional, der Swaan, Britt Van, additional, Lenarčič, Brigita, additional, Juliano, Luiz, additional, Mehta, Shwetal, additional, Van Noorden, Cornelis J.F., additional, and Lah, Tamara T., additional

Published
2017
Full Text
View/download PDF

3. Transmembrane protein CD9 is glioblastoma biomarker, relevant for maintenance of glioblastoma stem cells

Author

Podergajs, Neža, primary, Motaln, Helena, additional, Rajčević, Uroš, additional, Verbovšek, Urška, additional, Koršič, Marjan, additional, Obad, Nina, additional, Espedal, Heidi, additional, Vittori, Miloš, additional, Herold-Mende, Christel, additional, Miletic, Hrvoje, additional, Bjerkvig, Rolf, additional, and Turnšek, Tamara Lah, additional

Published
2015
Full Text
View/download PDF

5. Vloga matičnih celic pri napredovanju in zdravljenju glioma: The role of stem cells in glioma progression and therapy

Author

Lah Turnšek, Tamara, Motaln, Helena, Obrez, Mateja, and Verbovšek, Urška

Abstract

The concepts of tumour origin and stochastic nature of carcinogenesis are being challenged today by hierarchical models that predict the existence of cancer stem cells (CSCs), which are postulated as unique cell population capable of infinite self renewal, multilineage differentiation and having a higher resistance to conventional cancer therapy thus facilitating malignant growth and therapy resistance. Accordingly, successful treatment of adult brain tumourglioma and its most malignant stageglioblastoma multiforme (GBM), would require the elimination of CSCs to avoid tumour relapse. Yet, with available therapy (i.e. surgery) in GBMs this cannot be achieved, due to infiltrative growth of a subpopluation of GBM cells with highly expressed migratory genes (migratome) into the normal brain tissue. Besides CSCs a proven prerequisite for tumour development and progression, tumour bulk mass also comprises haematopoietic stem cells, endothelial progenitor cells and mesenchymal stem cells (MSCs). The role of these other types of stem cell was shown to largely depend on the tumour microenvironment, where their contradictory anti-tumour action was evidenced. Yet, the exact mechanisms and MSCs role in cell-mediated modulation of tumour behaviour via paracrine and direct interactions with GBM (stem) cells still remain unknown. Nevertheless these stem cells, particularly MSCs, may represent novel therapeutic vectors for enhanced target-site delivery of chemotherapeutics, which are urgently needed to improve efficiency of current glioma treatment. So far, cell therapy using MSCs appears promising, due to MSCs selective tumour tropism and their immuno-modulatory potential regarding treatment of GBM, which will be discussed in this review.

Published
2013

6. Analysis of Glioblastoma Patients' Plasma Revealed the Presence of MicroRNAs with a Prognostic Impact on Survival and Those of Viral Origin

Author

Herman, Ana, primary, Gruden, Kristina, additional, Blejec, Andrej, additional, Podpečan, Vid, additional, Motaln, Helena, additional, Rožman, Primož, additional, Hren, Matjaž, additional, Zupančič, Klemen, additional, Veber, Matija, additional, Verbovšek, Urška, additional, Lah Turnšek, Tamara, additional, Porčnik, Andrej, additional, Koršič, Marjan, additional, Knežević, Miomir, additional, and Jeras, Matjaž, additional

Published
2015
Full Text
View/download PDF

7. CD133+ and Nestin+ Glioma Stem-Like Cells Reside Around CD31+ Arterioles in Niches that Express SDF-1α, CXCR4, Osteopontin and Cathepsin K

Author

Hira, Vashendriya V. V., primary, Ploegmakers, Kimberley J., additional, Grevers, Frederieke, additional, Verbovšek, Urška, additional, Silvestre-Roig, Carlos, additional, Aronica, Eleonora, additional, Tigchelaar, Wikky, additional, Turnšek, Tamara Lah, additional, Molenaar, Remco J., additional, and Van Noorden, Cornelis J. F., additional

Published
2015
Full Text
View/download PDF

9. CD133+and Nestin+Glioma Stem-Like Cells Reside Around CD31+Arterioles in Niches that Express SDF-1α, CXCR4, Osteopontin and Cathepsin K

Author

Hira, Vashendriya V. V., Ploegmakers, Kimberley J., Grevers, Frederieke, Verbovšek, Urška, Silvestre-Roig, Carlos, Aronica, Eleonora, Tigchelaar, Wikky, Turnšek, Tamara Lah, Molenaar, Remco J., and Van Noorden, Cornelis J. F.

Abstract

Poor survival of high-grade glioma is at least partly caused by glioma stem-like cells (GSLCs) that are resistant to therapy. GSLCs reside in niches in close vicinity of endothelium. The aim of the present study was to characterize proteins that may be functional in the GSLC niche by performing immunohistochemistry on serial cryostat sections of human high-grade glioma samples. We have found nine niches in five out of five high-grade glioma samples that were all surrounding arterioles with CD31+endothelial cells and containing cellular structures that were CD133+and nestin+. All nine niches expressed stromal-derived factor-1α (SDF-1α), its receptor C-X-C chemokine receptor type 4 (CXCR4), osteopontin and cathepsin K. SDF-1α plays a role in homing of CXCR4+stem cells and leukocytes, whereas osteopontin and cathepsin K promote migration of cancer cells and leukocytes. Leukocyte-related markers, such as CD68, macrophage matrix metalloprotease-9, CD177 and neutrophil elastase were often but not always detected in the niches. We suggest that SDF-1α is involved in homing of CXCR4+GSLCs and leukocytes and that cathepsin K and osteopontin are involved in the migration of GSLCs out of the niches.

Published
2015
Full Text
View/download PDF

10. Transmembrane protein CD9 is glioblastoma biomarker, relevant for maintenance of glioblastoma stem cells.

Author

Podergajs N, Motaln H, Rajčević U, Verbovšek U, Koršič M, Obad N, Espedal H, Vittori M, Herold-Mende C, Miletic H, Bjerkvig R, and Turnšek TL

Subjects
Animals, Biomarkers, Tumor metabolism, Blotting, Western, Brain Neoplasms metabolism, Brain Neoplasms pathology, Cell Line, Tumor, Cell Proliferation genetics, Cell Survival genetics, Gene Expression Profiling methods, Gene Expression Regulation, Neoplastic, Glioblastoma metabolism, Glioblastoma pathology, Humans, Organ Culture Techniques, RNA Interference, Rats, Nude, Reverse Transcriptase Polymerase Chain Reaction, Survival Analysis, Tetraspanin 29 metabolism, Transplantation, Heterologous, Up-Regulation, Biomarkers, Tumor genetics, Brain Neoplasms genetics, Glioblastoma genetics, Neoplastic Stem Cells metabolism, Tetraspanin 29 genetics
Abstract

The cancer stem cell model suggests that glioblastomas contain a subpopulation of stem-like tumor cells that reproduce themselves to sustain tumor growth. Targeting these cells thus represents a novel treatment strategy and therefore more specific markers that characterize glioblastoma stem cells need to be identified. In the present study, we performed transcriptomic analysis of glioblastoma tissues compared to normal brain tissues revealing sensible up-regulation of CD9 gene. CD9 encodes the transmembrane protein tetraspanin which is involved in tumor cell invasion, apoptosis and resistance to chemotherapy. Using the public REMBRANDT database for brain tumors, we confirmed the prognostic value of CD9, whereby a more than two fold up-regulation correlates with shorter patient survival. We validated CD9 gene and protein expression showing selective up-regulation in glioblastoma stem cells isolated from primary biopsies and in primary organotypic glioblastoma spheroids as well as in U87-MG and U373 glioblastoma cell lines. In contrast, no or low CD9 gene expression was observed in normal human astrocytes, normal brain tissue and neural stem cells. CD9 silencing in three CD133+ glioblastoma cell lines (NCH644, NCH421k and NCH660h) led to decreased cell proliferation, survival, invasion, and self-renewal ability, and altered expression of the stem-cell markers CD133, nestin and SOX2. Moreover, CD9-silenced glioblastoma stem cells showed altered activation patterns of the Akt, MapK and Stat3 signaling transducers. Orthotopic xenotransplantation of CD9-silenced glioblastoma stem cells into nude rats promoted prolonged survival. Therefore, CD9 should be further evaluated as a target for glioblastoma treatment.

Published
2016
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results