ArticleOncotarget2017
High OCT4A levels drive tumorigenicity and metastatic potential of medulloblastoma cells.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Neurodegeneration-associated protein VAPB regulates proliferation in medulloblastoma.Scientific reports · 2023Article
- Article
- 3D spheroid models of paediatric SHH medulloblastoma mimic tumour biology, drug response and metastatic dissemination.Scientific reports · 2021Article
- Article
- Histone deacetylase inhibitors induce medulloblastoma cell death independent of HDACs recruited in REST repression complexes.Molecular genetics & genomic medicine · 2020Article
- Deregulation of Stemness-Related Genes in Endometriotic Mesenchymal Stem Cells: Further Evidence for Self-Renewal/Differentiation Imbalance.Iranian biomedical journal · 2020Article
- Human papillomavirus E7 binds Oct4 and regulates its activity in HPV-associated cervical cancers.PLoS pathogens · 2020Article
- Article
- Targeting MYCN in Molecularly Defined Malignant Brain Tumors.Frontiers in oncology · 2020Review
- Article
- Humanized Stem Cell Models of Pediatric Medulloblastoma Reveal an Oct4/mTOR Axis that Promotes Malignancy.Cell stem cell · 2019Article
- miR-367 as a therapeutic target in stem-like cells from embryonal central nervous system tumors.Molecular oncology · 2019Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Medulloblastoma is a highly aggressive pediatric brain tumor, in which sporadic expression of the pluripotency factor OCT4 has been recently correlated with poor patient survival. However the contribution of specific OCT4 isoforms to tumor aggressiveness is still poorly understood. Here, we report that medulloblastoma cells stably overexpressing the OCT4A isoform displayed enhanced clonogenic, tumorsphere generation, and invasion capabilities. Moreover, in an orthotopic metastatic model of medulloblastoma, OCT4A overexpressing cells generated more developed, aggressive and infiltrative tumors, with tumor-bearing mice attaining advanced metastatic disease and shorter survival rates. Pro-oncogenic OCT4A effects were expression-level dependent and accompanied by distinct chromosomal aberrations. OCT4A overexpression in medulloblastoma cells also induced a marked differential expression of non-coding RNAs, including poorly characterized long non-coding RNAs and small nucleolar RNAs. Altogether, our findings support the relevance of pluripotency-related factors in the aggravation of medulloblastoma traits classically associated with poor clinical outcome, and underscore the prognostic and therapeutic value of OCT4A in this challenging type of pediatric brain cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.