The role of octamer binding transcription factors in glioblastoma multiforme

Rooj, Arun K.; Bronisz, Agnieszka; Godlewski, Jakub

doi:10.1016/j.bbagrm.2016.03.003

Cited by 12 publications

(11 citation statements)

References 105 publications

(127 reference statements)

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“…Oct-3/4 also participates in the self-renewal of undifferentiated stem cells [18] and RT resistance [20]. Therefore, many investigators believe that EMT and cancer stemness are the main mechanisms for RT resistance [14,32,33].…”

Section: Discussionmentioning

confidence: 99%

Polyphenols Extracted from Artemisia annua L. Exhibit Anti-Cancer Effects on Radio-Resistant MDA-MB-231 Human Breast Cancer Cells by Suppressing Stem Cell Phenotype, β-Catenin, and MMP-9

Jung²,

Go³

et al. 2020

Molecules

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Artemisia annua L. has been reported to show anti-cancer activities. Here, we determined whether polyphenols extracted from Artemisia annua L. (pKAL) exhibit anti-cancer effects on radio-resistant MDA-MB-231 human breast cancer cells (RT-R-MDA-MB-231 cells), and further explored their molecular mechanisms. Cell viability assay and colony-forming assay revealed that pKAL inhibited cell proliferation on both parental and RT-R-MDA-MB-231 cells in a dose-dependent manner. The anti-proliferative effects of pKAL on RT-R-MDA-MB-231 cells were superior or similar to those on parental ones. Western blot analysis revealed that expressions of cluster of differentiation 44 (CD44) and Oct 3/4, matrix metalloproteinase-9 (MMP-9) and signal transducer and activator of transcription-3 (STAT-3) phosphorylation were significantly increased in RT-R-MDA-MB-231 cells compared to parental ones, suggesting that these proteins could be associated with RT resistance. pKAL inhibited the expression of CD44 and Oct 3/4 (CSC markers), and β-catenin and MMP-9 as well as STAT-3 phosphorylation of RT-R-MDA-MB-231. Regarding upstream signaling, the JNK or JAK2 inhibitor could inhibit STAT-3 activation in RT-R-MDA-MB-231 cells, but not augmented pKAL-induced anti-cancer effects. These findings suggest that c-Jun N-terminal kinase (JNK) or Janus kinase 2 (JAK2)/STAT3 signaling are not closely related to the anti-cancer effects of pKAL. In conclusion, this study suggests that pKAL exhibit anti-cancer effects on RT-R-MDA-MB-231 cells by suppressing CD44 and Oct 3/4, β-catenin and MMP-9, which appeared to be linked to RT resistance of RT-R-MDA-MB-231 cells.

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Section: Discussionmentioning

confidence: 99%

Polyphenols Extracted from Artemisia annua L. Exhibit Anti-Cancer Effects on Radio-Resistant MDA-MB-231 Human Breast Cancer Cells by Suppressing Stem Cell Phenotype, β-Catenin, and MMP-9

Jung²,

Go³

et al. 2020

Molecules

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“…Octamer binding transcription factors (OCTs) control early stages of developmental regulation. OCT7, SOX2, SALL2 and OLIG2 were demonstrated to be core transcription factors required for GBM reprogramming and transition of differentiated GBM to GSCs [ 32 ]. High expression level of OCT4 contributed to chemo-resistance [ 32 ].…”

Section: Introductionmentioning

confidence: 99%

Glioblastoma: new therapeutic strategies to address cellular and genomic complexity

Cai

Sughrue

2017

Oncotarget

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Glioblastoma (GBM) is the most invasive and devastating primary brain tumor with a median overall survival rate about 18 months with aggressive multimodality therapy. Its unique characteristics of heterogeneity, invasion, clonal populations maintaining stem cell-like cells and recurrence, have limited responses to a variety of therapeutic approaches, and have made GBM the most difficult brain cancer to treat. A great effort and progress has been made to reveal promising molecular mechanisms to target therapeutically. Especially with the emerging of new technologies, the mechanisms underlying the pathology of GBM are becoming more clear. The purpose of this review is to summarize the current knowledge of molecular mechanisms of GBM and highlight the novel strategies and concepts for the treatment of GBM.

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“…As an example of such action by glioblastoma cells, the efforts by our group provided the evidence of glucose availability-regulated feedback loop that promotes either proliferative or migratory mode, depending on the microenvironmental context. Here we argue that the adaptation to stress and the remodeling of immune surveillance drive the survival and proliferation of glioblastoma cells in hypoxic zones and that such strategy is equally, if not more important as the behavioral transition [45,46].…”

Section: Discussionmentioning

confidence: 92%

Hypoxic Roadmap of Glioblastoma—Learning about Directions and Distances in the Brain Tumor Environment

Bronisz

Salińska

Chiocca

et al. 2020

Cancers

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Malignant brain tumor—glioblastoma is not only difficult to treat but also hard to study and model. One of the reasons for these is their heterogeneity, i.e., individual tumors consisting of cancer cells that are unlike each other. Such diverse cells can thrive due to the simultaneous co-evolution of anatomic niches and adaption into zones with distorted homeostasis of oxygen. It dampens cytotoxic and immune therapies as the response depends on the cellular composition and its adaptation to hypoxia. We explored what transcriptome reposition strategies are used by cells in the different areas of the tumor. We created the hypoxic map by differential expression analysis between hypoxic and cellular features using RNA sequencing data cross-referenced with the tumor’s anatomic features (Ivy Glioblastoma Atlas Project). The molecular functions of genes differentially expressed in the hypoxic regions were analyzed by a systematic review of the gene ontology analysis. To put a hypoxic niche signature into a clinical context, we associated the model with patients’ survival datasets (The Cancer Genome Atlas). The most unique class of genes in the hypoxic area of the tumor was associated with the process of autophagy. Both hypoxic and cellular anatomic features were enriched in immune response genes whose, along with autophagy cluster genes, had the power to predict glioblastoma patient survival. Our analysis revealed that transcriptome responsive to hypoxia predicted worse patients’ outcomes by driving tumor cell adaptation to metabolic stress and immune escape.

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The role of octamer binding transcription factors in glioblastoma multiforme

Cited by 12 publications

References 105 publications

Polyphenols Extracted from Artemisia annua L. Exhibit Anti-Cancer Effects on Radio-Resistant MDA-MB-231 Human Breast Cancer Cells by Suppressing Stem Cell Phenotype, β-Catenin, and MMP-9

Polyphenols Extracted from Artemisia annua L. Exhibit Anti-Cancer Effects on Radio-Resistant MDA-MB-231 Human Breast Cancer Cells by Suppressing Stem Cell Phenotype, β-Catenin, and MMP-9

Glioblastoma: new therapeutic strategies to address cellular and genomic complexity

Hypoxic Roadmap of Glioblastoma—Learning about Directions and Distances in the Brain Tumor Environment

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