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All-trans retinoic acid fosters the multifarious U87MG cell line as a model of glioblastoma

All-trans retinoic acid fosters the multifarious U87MG cell line as a model of glioblastoma

Pokorná, Markéta, Hudec, Michael, Juříčková, Iva, Michael, Vácha, Zdeňka, Polívková, Viera, Kútna, Jan, Pala, Ovsepian, Saak V., Marie, Černá and Valerie Bríd, O'Leary (2021) All-trans retinoic acid fosters the multifarious U87MG cell line as a model of glioblastoma. Brain Sciences, 11 (6):812. ISSN 2076-3425 (Online) (doi:10.3390/brainsci11060812)

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Abstract

Glioblastoma multiforme (GBM) is a primary brain cancer of poor prognosis, with existing treatments remaining essentially palliative. Current GBM therapy fails due to rapid reappearance of the heterogeneous neoplasm, with models suggesting that the recurrent growth is from treatment-resistant glioblastoma stem-like cells (GSCs). Whether GSCs depend on survival/proliferative cues from their surrounding microenvironmental niche, particularly surrounding the leading edge after treatment remains unknown. Simulating human GBM in the laboratory relies on representative cell lines and xenograft models for translational medicine. Due to U87MG source discrepancy and differential proliferation responses to retinoic acid treatment, this study highlights the challenges faced by laboratory scientists working with this representative GBM cell line. Investigating the response to all trans-retinoic acid (ATRA) revealed its sequestering of the prominin-1 stem cell marker. ICAM-1 universally present throughout U87MG was enhanced by ATRA, of interest for chemotherapy targeting studies. ATRA triggered diverse expression patterns of long non-coding RNAs PARTICLE and GAS5 in the leading edge and established monolayer growth zone microenvironment. Karyotyping confirmed the female origin of U87MG sourced from Europe. Passaging U87MG revealed the presence of chromosomal anomalies reflective of structural genomic alterations in this glioblastoma cell line. All evidence considered, this study exposes further phenotypic nuances of U87MG which may belie researchers seeking data contributing towards the elusive cure for GBM.

Item Type: Article
Additional Information: © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
Uncontrolled Keywords: chromosome, lncRNA, CD54, prominin-1, ATRA, brain cancer
Subjects: Q Science > Q Science (General)
Faculty / School / Research Centre / Research Group: Faculty of Engineering & Science
Faculty of Engineering & Science > School of Science (SCI)
Last Modified: 23 Nov 2021 11:18
URI: http://gala.gre.ac.uk/id/eprint/34271

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