Prominin-1 (CD133) Defines Both Stem and Non-Stem Cell Populations in CNS Development and Gliomas

Olausson, Karl Holmberg; Maire, Cécile L.; Haidar, Sam; Ling, Jason; Learner, Emily R; Nistér, Monica; Ligon, Keith L.

doi:10.1371/journal.pone.0106694

Cited by 35 publications

(24 citation statements)

References 46 publications

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“…It has previously been reported that CD133 mRNA expression is negatively associated with IDH1 mutation and the G-CIMP group of Proneural GBMs [40]. Our analyses confirm this observation (p- value 0.006, t-test) (Figure S5C).…”

Section: Resultssupporting

confidence: 89%

Coexpression analysis of CD133 and CD44 identifies Proneural and Mesenchymal subtypes of glioblastoma multiforme

et al. 2015

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Accumulating evidence suggests that the stem cell markers CD133 and CD44 indicate molecular subtype in Glioblastoma Multiforme (GBM). Gene coexpression analysis of The Cancer Genome Atlas GBM dataset was undertaken to compare markers of the Glioblastoma Stem-Progenitor Cell (GSPC) phenotype. Pearson correlation identified genes coexpressed with stem cell markers, which were then used to build a gene signature that classifies patients based on a CD133 coexpression module signature (CD133-M) or CD44-M subtype. CD133-M tumors were enriched for the Proneural (PN) GBM subtype compared to Mesenchymal (MES) subtype for CD44-M tumors. Gene set enrichment identified DNA replication/cell cycle genes in the CD133-M and invasion/migration in CD44-M, while functional experiments showed enhanced cellular growth in CD133 expressing cells and enhanced invasion in cells expressing CD44. As with the 4 major molecular subtypes of GBM, there was no long-term survival difference between CD44-M and CD133-M patients, although CD44-M patients responded better to temozolomide while CD133-M patients benefited from radiotherapy. The use of a targeted coexpression approach to predict functional properties of surface marker expressing cells is novel, and in the context of GBM, supports accumulating evidence that CD133 and CD44 protein marker expression correlates with molecular subtype.

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Section: Resultssupporting

confidence: 89%

Coexpression analysis of CD133 and CD44 identifies Proneural and Mesenchymal subtypes of glioblastoma multiforme

et al. 2015

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“…To do so, we utilized primary patient-derived glioblastoma tumor-initiating cells that are propagated as neurospheres in neural stem cell media to maintain their ‘stem cell-like’ properties. These cells are highly tumorigenic in vivo , and form aggressive glioblastomas upon intracranial injection into recipient mice 38 . We treated cultures of glioblastoma tumor-initiating cell lines derived from four independent patients with CVT-313, and monitored Sox2 levels.…”

Section: Resultsmentioning

confidence: 99%

G1 cyclins link proliferation, pluripotency and differentiation of embryonic stem cells

et al. 2017

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Progression of mammalian cells through the G1 and S phases of the cell cycle is driven by D-type and E-type cyclins. According to the current models, at least one of these cyclin families must be present to allow cell proliferation. Here, we show that several cell types can proliferate in the absence of all G1 cyclins. However, upon ablation of G1 cyclins, embryonic stem (ES) cells attenuated their pluripotent characteristics, with majority of cells acquiring the trophectodermal cell fate. We established that G1 cyclins, together with their associated cyclin-dependent kinases (CDKs) phosphorylate and stabilize core pluripotency factors Nanog, Sox2 and Oct4. Treatment of murine ES cells, patient-derived glioblastoma tumor-initiating cells, or triple-negative breast cancer cells with a CDK-inhibitor strongly decreased Sox2 and Oct4 levels. Our findings suggest that CDK-inhibition might represent an attractive therapeutic strategy by targeting glioblastoma tumor-initiating cells, which depend on Sox2 to maintain their tumorigenic potential.

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“…The cell surface antigen CD133 is notoriously expressed in physiological neural stem cells, and has also been considered a suitable marker to identify GBM CSC fractions [2,109,110].…”

Section: Nps Conjugated To Cd133 Antibodymentioning

confidence: 99%

Targeting Glioblastoma with the Use of Phytocompounds and Nanoparticles

et al. 2015

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Glioblastoma multiforme (GBM) are extremely lethal and still poorly treated primary brain tumors, characterized by the presence of highly tumorigenic cancer stem cell (CSC) subpopulations, considered responsible for tumor relapse. In order to successfully eradicate GBM growth and recurrence, new anti-cancer strategies selectively targeting CSCs should be designed. CSCs might be eradicated by targeting some of their cell surface markers and transporters, inducing their differentiation, impacting their hyper-glycolytic metabolism, inhibiting CSC-related signaling pathways and/or by targeting their microenvironmental niche. In this regard, phytocompounds such as curcumin, isothiocyanates, resveratrol and epigallocatechin-3-gallate have been shown to prevent or reverse cancer-related epigenetic dysfunctions, reducing tumorigenesis, preventing metastasis and/or increasing chemotherapy and radiotherapy efficacy. However, the actual bioavailability and metabolic processing of phytocompounds is generally unknown, and the presence of the blood brain barrier often represents a limitation to glioma treatments. Nowadays, nanoparticles (NPs) can be loaded with therapeutic compounds such as phytochemicals, improving their bioavailability and their targeted delivery within the GBM tumor bulk. Moreover, NPs can be designed to increase their tropism and specificity toward CSCs by conjugating their surface with antibodies specific for CSC antigens, with ligands or with glucose analogues. Here we discuss the use of phytochemicals as anti-glioma agents and the applicability of phytochemical-loaded NPs as drug delivery systems to target GBM. Additionally, we provide some examples on how NPs can be specifically formulated to improve CSC targeting.

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Prominin-1 (CD133) Defines Both Stem and Non-Stem Cell Populations in CNS Development and Gliomas

Cited by 35 publications

References 46 publications

Coexpression analysis of CD133 and CD44 identifies Proneural and Mesenchymal subtypes of glioblastoma multiforme

Coexpression analysis of CD133 and CD44 identifies Proneural and Mesenchymal subtypes of glioblastoma multiforme

G1 cyclins link proliferation, pluripotency and differentiation of embryonic stem cells

Targeting Glioblastoma with the Use of Phytocompounds and Nanoparticles

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