scholarly journals ABCG2 regulates self-renewal and stem cell marker expression but not tumorigenicity or radiation resistance of glioma cells

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Boyoung Wee ◽  
Alexander Pietras ◽  
Tatsuya Ozawa ◽  
Elena Bazzoli ◽  
Ondrej Podlaha ◽  
...  
Keyword(s):  
Stem Cell ◽  
Radiation Resistance ◽  
Glioma Cells ◽  
Stem Cell Marker ◽  
Cell Marker ◽  
Self Renewal ◽  
Marker Expression

scholarly journals Differential SOD2 and GSTZ1 profiles contribute to contrasting dental pulp stem cell susceptibilities to oxidative damage and premature senescence

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Nadia Y. A. Alaidaroos ◽  
Amr Alraies ◽  
Rachel J. Waddington ◽  
Alastair J. Sloan ◽  
Ryan Moseley
Keyword(s):  
Stem Cell ◽  
Regenerative Medicine ◽  
Oxidative Damage ◽  
Dental Pulp ◽  
Stem Cell Marker ◽  
Significant Heterogeneity ◽  
Premature Senescence ◽  
Cell Marker ◽  
Marker Expression ◽  
The Impact

Abstract Background Dental pulp stem cells (DPSCs) are increasingly being advocated as viable cell sources for regenerative medicine-based therapies. However, significant heterogeneity in DPSC expansion and multi-potency capabilities are well-established, attributed to contrasting telomere profiles and susceptibilities to replicative senescence. As DPSCs possess negligible human telomerase (hTERT) expression, we examined whether intrinsic differences in the susceptibilities of DPSC sub-populations to oxidative stress-induced biomolecular damage and premature senescence further contributed to this heterogeneity, via differential enzymic antioxidant capabilities between DPSCs. Methods DPSCs were isolated from human third molars by differential fibronectin adhesion, and positive mesenchymal (CD73/CD90/CD105) and negative hematopoietic (CD45) stem cell marker expression confirmed. Isolated sub-populations were expanded in H2O2 (0–200 μM) and established as high or low proliferative DPSCs, based on population doublings (PDs) and senescence (telomere lengths, SA-β-galactosidase, p53/p16INK4a/p21waf1/hTERT) marker detection. The impact of DPSC expansion on mesenchymal, embryonic, and neural crest marker expression was assessed, as were the susceptibilities of high and low proliferative DPSCs to oxidative DNA and protein damage by immunocytochemistry. Expression profiles for superoxide dismutases (SODs), catalase, and glutathione-related antioxidants were further compared between DPSC sub-populations by qRT-PCR, Western blotting and activity assays. Results High proliferative DPSCs underwent > 80PDs in culture and resisted H2O2−induced senescence (50–76PDs). In contrast, low proliferative sub-populations exhibited accelerated senescence (4–32PDs), even in untreated controls (11-34PDs). While telomere lengths were largely unaffected, certain stem cell marker expression declined with H2O2 treatment and expansion. Elevated senescence susceptibilities in low proliferative DPSC (2–10PDs) were accompanied by increased oxidative damage, absent in high proliferative DPSCs until 45–60PDs. Increased SOD2/glutathione S-transferase ζ1 (GSTZ1) expression and SOD activities were identified in high proliferative DPSCs (10–25PDs), which declined during expansion. Low proliferative DPSCs (2–10PDs) exhibited inferior SOD, catalase and glutathione-related antioxidant expression/activities. Conclusions Significant variations exist in the susceptibilities of DPSC sub-populations to oxidative damage and premature senescence, contributed to by differential SOD2 and GSTZ1 profiles which maintain senescence-resistance/stemness properties in high proliferative DPSCs. Identification of superior antioxidant properties in high proliferative DPSCs enhances our understanding of DPSC biology and senescence, which may be exploited for selective sub-population screening/isolation from dental pulp tissues for regenerative medicine-based applications.

Cancer stem cell marker expression in hepatocellular carcinoma and liver metastases is not sufficient as single prognostic parameter

2009 ◽  
Vol 275 (2) ◽  
pp. 185-193 ◽  
Author(s):  
Alexei V. Salnikov ◽  
Grace Kusumawidjaja ◽  
Vanessa Rausch ◽  
Helge Bruns ◽  
Wolfgang Gross ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Liver Metastases ◽  
Stem Cell Marker ◽  
Cancer Stem Cell Marker ◽  
Cell Marker ◽  
Prognostic Parameter ◽  
Marker Expression

628 Stem cell marker expression profile in colon cancer xenografts and their corresponding cell lines

2010 ◽  
Vol 8 (7) ◽  
pp. 197
Author(s):  
M. Schneider ◽  
A. Maier ◽  
G. Kelter ◽  
A. Korrat ◽  
H.H. Fiebig ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Stem Cell ◽  
Cell Lines ◽  
Expression Profile ◽  
Stem Cell Marker ◽  
Cell Marker ◽  
Marker Expression

Mesenchymal Stem Cell Marker Expression in Periapical Abscess

2019 ◽  
Vol 45 (6) ◽  
pp. 716-723 ◽  
Author(s):  
Carlos Estrela ◽  
Paulo Otávio Carmo Souza ◽  
Mateus Gehrke Barbosa ◽  
Artur Aburad de Carvalhosa ◽  
Aline Carvalho Batista ◽  
...  
Keyword(s):  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Stem Cell Marker ◽  
Cell Marker ◽  
Periapical Abscess ◽  
Marker Expression

scholarly journals MSI1 Promotes the Expression of the GBM Stem Cell Marker CD44 by Impairing miRNA-Dependent Degradation

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3654
Author(s):  
Rebecca Pötschke ◽  
Jacob Haase ◽  
Markus Glaß ◽  
Sebastian Simmermacher ◽  
Claudia Misiak ◽  
...  
Keyword(s):  
Stem Cell ◽  
Stem Cell Marker ◽  
Mrna Turnover ◽  
Stem Cell Markers ◽  
Dependent Manner ◽  
Cell Marker ◽  
Cell Models ◽  
Comprehensive Understanding ◽  
Self Renewal ◽  
First Time

The stem cell marker Musashi1 (MSI1) is highly expressed during neurogenesis and in glioblastoma (GBM). MSI1 promotes self-renewal and impairs differentiation in cancer and non-malignant progenitor cells. However, a comprehensive understanding of its role in promoting GBM-driving networks remains to be deciphered. We demonstrate that MSI1 is highly expressed in GBM recurrences, an oncologist’s major defiance. For the first time, we provide evidence that MSI1 promotes the expression of stem cell markers like CD44, co-expressed with MSI1 within recurrence-promoting cells at the migrating front of primary GBM samples. With GBM cell models of pediatric and adult origin, including isolated primary tumorspheres, we show that MSI1 promotes stem cell-like characteristics. Importantly, it impairs CD44 downregulation in a 3′UTR- and miRNA-dependent manner by controlling mRNA turnover. This regulation is disturbed by the previously reported MSI1 inhibitor luteolin, providing further evidence for a therapeutic target potential of MSI1 in GBM treatment.

Sign in / Sign up

Export Citation Format

Share Document