scholarly journals HMGA2 sustains self-renewal and invasiveness of glioma-initiating cells

Oncotarget ◽  
2016 ◽  
Vol 7 (28) ◽  
pp. 44365-44380 ◽  
Author(s):  
Xiaoling Zhong ◽  
Xuan Liu ◽  
Yamu Li ◽  
Man Cheng ◽  
Wen Wang ◽  
...  
Keyword(s):  
Self Renewal ◽  
Glioma Initiating Cells

scholarly journals Cathepsin B and uPAR regulate self-renewal of glioma-initiating cells through GLI-regulated Sox2 and Bmi1 expression

2012 ◽  
Vol 34 (3) ◽  
pp. 550-559 ◽  
Author(s):  
Sreelatha Gopinath ◽  
RamaRao Malla ◽  
Kiranmai Alapati ◽  
Bharathi Gorantla ◽  
Meena Gujrati ◽  
...  
Keyword(s):  
Cathepsin B ◽  
Self Renewal ◽  
Glioma Initiating Cells ◽  
Bmi1 Expression

scholarly journals AURKA Governs Self-Renewal Capacity in Glioma-Initiating Cells via Stabilization/Activation of β-catenin/Wnt Signaling

2013 ◽  
Vol 11 (9) ◽  
pp. 1101-1111 ◽  
Author(s):  
Zhibo Xia ◽  
Ping Wei ◽  
Heng Zhang ◽  
Zhiming Ding ◽  
Lixuan Yang ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Self Renewal ◽  
Glioma Initiating Cells

PTEN status is related to cell proliferation and self-renewal independent of CD133 phenotype in the glioma-initiating cells

2010 ◽  
Vol 349 (1-2) ◽  
pp. 149-157 ◽  
Author(s):  
Ru-Bin Cheng ◽  
Rui-Juan Ma ◽  
Zhao-Kai Wang ◽  
Shan-Jun Yang ◽  
Xiang-Zhi Lin ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Self Renewal ◽  
Glioma Initiating Cells

scholarly journals BOT-02 2-METHYLTHIO MODIFICATION OF N6-ISOPENTENYLADENOSINE IN MITOCHONDRIAL TRNAS BY CDK5RAP1 PROMOTES THE MAINTENANCE OF GLIOMA-INITIATING CELLS

2019 ◽  
Vol 1 (Supplement_2) ◽  
pp. ii12-ii12
Author(s):  
Takahiro Yamamoto ◽  
Atsushi Fujimura ◽  
Wei Fan-Yan ◽  
Keitarou Kai ◽  
Tatsuya Takezaki ◽  
...  
Keyword(s):  
Translational Control ◽  
Cytotoxic Effect ◽  
Regulatory Subunit ◽  
Mitochondrial Translation ◽  
Mt Dna ◽  
Self Renewal ◽  
Glioma Initiating Cells ◽  
Undifferentiated State ◽  
Tumorigenic Potential ◽  
Elevated Activity

Abstract 2-Methylthio-N6-isopentenyl modification of adenosine (ms2i6A) is an evolutionally conserved modification that is found in mitochondrial (mt)-tRNAs. Cdk5 regulatory subunit-associated protein 1 (CDK5RAP1) specifically converts N6-isopentenyladenosine (i6A) to ms2i6A at position A37 of four mt-DNA-encoded tRNAs, and the modification regulates efficient mitochondrial translation and energy metabolism in mammals. Here, we report that the ms2 conversion mediated by CDK5RAP1 in mt-tRNAs is required to sustain glioma-initiating cell (GIC)-related traits. CDK5RAP1 maintained the self-renewal capacity, undifferentiated state, and tumorigenic potential of GICs. This regulation was not related to the translational control of mt-proteins. CDK5RAP1 abrogated the antitumor effect of i6A by converting i6A to ms2i6A and protected GICs from excessive autophagy triggered by i6A. The elevated activity of CDK5RAP1 contributed to the amelioration of the cytotoxic effect of i6A and promoted GIC maintenance. The hypoxic microenvironment in the tumor core activated CDK5RAP1, whose activity was inversely correlated with the oxygen concentration because of two [4Fe-4S] clusters in the enzyme. This work demonstrates that CDK5RAP1 is crucial for the detoxification of endogenous i6A and that GICs readily utilize this mechanism for survival.

scholarly journals FSMP-01. ID1 MEDIATES ONE-CARBON MEDIATED PURINE SYNTHESIS IN GLIOBLASTOMA

2021 ◽  
Vol 3 (Supplement_1) ◽  
pp. i16-i16
Author(s):  
Kimia Ghannad-Zadeh ◽  
Megan Wu ◽  
Taylor Wilson ◽  
Robert Flick ◽  
Sunit Das
Keyword(s):  
De Novo ◽  
Regulatory Protein ◽  
Metabolic Reprogramming ◽  
Glioblastoma Cells ◽  
Self Renewal ◽  
Purine Synthesis ◽  
Glioma Initiating Cells ◽  
Effective Combination ◽  
Transcriptional Regulatory ◽  
One Carbon Metabolism

Abstract Inhibitor of DNA-binding-1 (ID1) is a transcriptional regulatory protein involved in maintenance of self-renewal and inhibition of differentiation, and acts as a key regulator of tumorigenesis in glioblastoma. Studies suggest that de novo purine synthesis is essential for the maintenance of rapid proliferation rates in glioma initiating cells. We hypothesise that ID1 plays a role in reprogramming one-carbon mediated de novo purine synthesis, thereby metabolically contributing to the tumorigenic advantage seen in ID1-high glioblastoma cells. The effect of ID1 regulation on metabolic reprogramming of glioblastoma was studied using ID1-knockout U251 glioblastoma cell lines. Protein expression analysis and liquid chromatography mass-spectrometry were respectively used to assess expression and concentration of metabolic enzymes and intermediates of one-carbon and de novo purine synthesis pathways. CD44 expression was analyzed as a marker of cancer stem cells. The expression of DHFR and MTHFD2 was significantly decreased after ID1 knockout. Furthermore, PAICS expression, and overall concentration of IMP, AMP, GMP, and ATP were reduced after ID1 knockout. ID1 expression in glioblastoma tumor xenografts was associated with positive expression of one-carbon metabolism and purine synthesis enzymes, while ID1-/- cells within the same xenograft had significantly reduced expression of these enzymes. The expression of CD44 was reduced after ID1 knockout. This data suggests that ID1 mediates an increase in one-carbon mediated de novo purine synthesis, thereby regulating metabolic reprogramming in glioblastoma cells. The correlation between CD44 and ID1 expression provides further support that ID1 maintains a less differentiated phenotype in a subset of glioblastoma cells, and metabolic reprogramming is one of the mechanisms through which this phenotype, and the capacity for self-renewal are maintained. Further elucidation of the mechanisms through which ID1 mediates metabolic reprograming of glioblastoma cells can lead to developing effective combination therapies coupling chemotherapeutic strategies with targeting of metabolic programs used by cancer initiating cells.

scholarly journals BRD4 regulates self‐renewal ability and tumorigenicity of glioma‐initiating cells by enrichment in the Notch1 promoter region

2020 ◽  
Vol 10 (6) ◽  
Author(s):  
Zhennan Tao ◽  
Xuetao Li ◽  
Hao Wang ◽  
Guangliang Chen ◽  
Zibin Feng ◽  
...  
Keyword(s):  
Promoter Region ◽  
Self Renewal ◽  
Glioma Initiating Cells

scholarly journals NKX2.2 Suppresses Self-Renewal of Glioma-Initiating Cells

2010 ◽  
Vol 71 (3) ◽  
pp. 1135-1145 ◽  
Author(s):  
Teruyuki Muraguchi ◽  
Shingo Tanaka ◽  
Daisuke Yamada ◽  
Akira Tamase ◽  
Mitsutoshi Nakada ◽  
...  
Keyword(s):  
Self Renewal ◽  
Glioma Initiating Cells
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