ArticleOncotarget2015
Down regulation of Akirin-2 increases chemosensitivity in human glioblastomas more efficiently than Twist-1.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- ZBTB7A-mediated regulation of astrocytic glycolysis in neurodegenerative diseases: insights from literature review and bioinformatics prediction.Frontiers in aging neuroscience · 2026Review
- Transcranial direct current stimulation enhances the protective effect of isoflurane preconditioning on cerebral ischemia/reperfusion injury: A new mechanism associated with the nuclear protein Akirin2.CNS neuroscience & therapeutics · 2024Article
- Role of nuclear protein Akirin in the modulation of female reproduction inFrontiers in physiology · 2024Article
- Identification of AKIRIN2 as a potential biomarker and correlation with immunotherapy in gastric adenocarcinoma by integrated bioinformatics analysis.Scientific reports · 2022Article
- Article
- Systematic Analysis of Molecular Subtypes and Immune Prediction Based on CD8 T Cell Pattern Genes Based on Head and Neck Cancer.Journal of oncology · 2022Article
- Role of ZBTB7A zinc finger in tumorigenesis and metastasis.Molecular biology reports · 2021Review
- Akirin proteins in development and disease: critical roles and mechanisms of action.Cellular and molecular life sciences : CMLS · 2020Review
- Akirin2 is modulated by miR-490-3p and facilitates angiogenesis in cholangiocarcinoma through the IL-6/STAT3/VEGFA signaling pathway.Cell death & disease · 2019Article
- Signaling pathways and mesenchymal transition in pediatric high-grade glioma.Cellular and molecular life sciences : CMLS · 2018Review
- Characterization of theFrontiers in physiology · 2018Article
- Functional Evolution of Subolesin/Akirin.Frontiers in physiology · 2018Review
- Akirin2 is essential for the formation of the cerebral cortex.Neural development · 2016Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Twist-1 transcription factor and its interacting protein Akirin-2 regulate apoptosis. We found that in glioblastomas, highly malignant brain tumors, Akirin-2 and Twist-1 were expressed in glial fibrillary acidic protein positive tumor regions as well as in tumor endothelial cells and infiltrating macrophages / microglia. Temozolomide (TMZ) induced the expression of both molecules, partly shifting their nuclear to cytosolic localization. The knock-down (kd) of Akirin-2 increased the activity of cleaved (c)Caspase-3/-7, the amounts of cCaspases-3, -7 and cPARP-1 and resulted in an increased number of apoptotic cells after TMZ exposure. Glioblastoma cells containing decreased amounts of Akirin-2 after kd contained increased amounts of cCaspase-3 as determined by the ImageStreamx Mark II technology. For Twist-1, similar results were obtained with the exception that the combination of TMZ treatment and Twist-1 kd failed to significantly reduce chemoresistance compared with controls. This could be attributed to a cell population containing only slightly increased cCaspase-3 together with decreased Twist-1 levels, which was clearly larger than the respective population observed under Akirin-2 kd. Our results showed that, compared with Twist-1, Akirin-2 is the more promising target for RNAi strategies antagonizing Twist-1/Akirin-2 facilitated glioblastoma cell survival.
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