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OMRT-11. The effect of microenvironment on glioblastoma stem cells therapeutic resistance
Epithelial-to-mesenchymal transition (EMT) is an essential molecular and cellular process in physiologic processes and invasion of various types of carcinoma and glioblastoma (GBM) cells. EMT is activated and regulated by specific endogenous triggers in complex network of intercellular interactions...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8255438/ http://dx.doi.org/10.1093/noajnl/vdab070.035 |
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author | Turnsek, Tamara Lah Breznik, Barbara Majc, Bernarda Novak, Metka Porčnik, Andrej Habič, Anamarija Mlinar, Mateja Bošnjak, Roman |
author_facet | Turnsek, Tamara Lah Breznik, Barbara Majc, Bernarda Novak, Metka Porčnik, Andrej Habič, Anamarija Mlinar, Mateja Bošnjak, Roman |
author_sort | Turnsek, Tamara Lah |
collection | PubMed |
description | Epithelial-to-mesenchymal transition (EMT) is an essential molecular and cellular process in physiologic processes and invasion of various types of carcinoma and glioblastoma (GBM) cells. EMT is activated and regulated by specific endogenous triggers in complex network of intercellular interactions and signaling pathways. The hallmark of cancer-linked EMT are intermediate states that show notable cell plasticity, characteristic of cancer stem cells (CSCs), including glioblastoma stem cells – GSCs. GSCs resistance to irradiation (IR) and temozolomide (TMZ) chemotherapy is responsible for early relapses, even at distant brain sites. As GSCs are mostly homing to their “niches” as slowly-dividing GSC-subtype, mimicking a proneural-like non- invasive phenotype PN-genotype, we assume that this, by undergoing an EMT-like transition, GSCs are-reprogrammed to an invasive mesenchymal (MES) GBs/GSCs phenotype in a processes, called PMT (1). However, it is not known, if and by which environmental cues within the niche, this transition of GSCs is induced in vivo. In this work, we are presenting the transriptome data obtained when we exposed GSC spheroids to irradiation alone, TMZ alone and to the combined treatment in vitro and compared their differential genetic fingerprints related to EMT/PMT transition to the GSCs PMT transition, when embedded in their natural microenvironment in the GBM organoid model. The differential gene expression upon GSCs therapeutic perturbation (when alone and vs in the tumoroid microenvironment) will reveal the effects of the major candidate genes, associated with micronevironmendt stromal cells and matrix are contributing their observed EMT/PMT transition of GSCs in vivo. •1. Majc, B., Sever, T., Zarić, M, Breznik, B., Turk, B, Lah Turnšek, T. Epithelial- to-mesenchymal transition as the driver of changing carcinoma and glioblastoma microenvironment. DOI: 10.1016/j.bbamcr.2020.118782 |
format | Online Article Text |
id | pubmed-8255438 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-82554382021-07-06 OMRT-11. The effect of microenvironment on glioblastoma stem cells therapeutic resistance Turnsek, Tamara Lah Breznik, Barbara Majc, Bernarda Novak, Metka Porčnik, Andrej Habič, Anamarija Mlinar, Mateja Bošnjak, Roman Neurooncol Adv Supplement Abstracts Epithelial-to-mesenchymal transition (EMT) is an essential molecular and cellular process in physiologic processes and invasion of various types of carcinoma and glioblastoma (GBM) cells. EMT is activated and regulated by specific endogenous triggers in complex network of intercellular interactions and signaling pathways. The hallmark of cancer-linked EMT are intermediate states that show notable cell plasticity, characteristic of cancer stem cells (CSCs), including glioblastoma stem cells – GSCs. GSCs resistance to irradiation (IR) and temozolomide (TMZ) chemotherapy is responsible for early relapses, even at distant brain sites. As GSCs are mostly homing to their “niches” as slowly-dividing GSC-subtype, mimicking a proneural-like non- invasive phenotype PN-genotype, we assume that this, by undergoing an EMT-like transition, GSCs are-reprogrammed to an invasive mesenchymal (MES) GBs/GSCs phenotype in a processes, called PMT (1). However, it is not known, if and by which environmental cues within the niche, this transition of GSCs is induced in vivo. In this work, we are presenting the transriptome data obtained when we exposed GSC spheroids to irradiation alone, TMZ alone and to the combined treatment in vitro and compared their differential genetic fingerprints related to EMT/PMT transition to the GSCs PMT transition, when embedded in their natural microenvironment in the GBM organoid model. The differential gene expression upon GSCs therapeutic perturbation (when alone and vs in the tumoroid microenvironment) will reveal the effects of the major candidate genes, associated with micronevironmendt stromal cells and matrix are contributing their observed EMT/PMT transition of GSCs in vivo. •1. Majc, B., Sever, T., Zarić, M, Breznik, B., Turk, B, Lah Turnšek, T. Epithelial- to-mesenchymal transition as the driver of changing carcinoma and glioblastoma microenvironment. DOI: 10.1016/j.bbamcr.2020.118782 Oxford University Press 2021-07-05 /pmc/articles/PMC8255438/ http://dx.doi.org/10.1093/noajnl/vdab070.035 Text en © The Author(s) 2021. Published by Oxford University Press, the Society for Neuro-Oncology and the European Association of Neuro-Oncology. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Supplement Abstracts Turnsek, Tamara Lah Breznik, Barbara Majc, Bernarda Novak, Metka Porčnik, Andrej Habič, Anamarija Mlinar, Mateja Bošnjak, Roman OMRT-11. The effect of microenvironment on glioblastoma stem cells therapeutic resistance |
title | OMRT-11. The effect of microenvironment on glioblastoma stem cells therapeutic resistance |
title_full | OMRT-11. The effect of microenvironment on glioblastoma stem cells therapeutic resistance |
title_fullStr | OMRT-11. The effect of microenvironment on glioblastoma stem cells therapeutic resistance |
title_full_unstemmed | OMRT-11. The effect of microenvironment on glioblastoma stem cells therapeutic resistance |
title_short | OMRT-11. The effect of microenvironment on glioblastoma stem cells therapeutic resistance |
title_sort | omrt-11. the effect of microenvironment on glioblastoma stem cells therapeutic resistance |
topic | Supplement Abstracts |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8255438/ http://dx.doi.org/10.1093/noajnl/vdab070.035 |
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