AI Article Synopsis
- Glioblastoma and gliomas have various histopathologic subtypes linked to glioma stem cells (GSCs) that contribute to tumor growth and self-renewal.
- GSCs are regulated by complex epigenetic mechanisms involving non-coding RNAs (ncRNAs), which play crucial roles in cancer development by acting as oncogenes or tumor suppressors.
- Recent research highlights the impact of ncRNAs on glioma progression, especially regarding cancer stem cells, suggesting their potential as biomarkers and therapeutic targets in clinical settings.
Article Abstract
Glioblastoma and gliomas can have a wide range of histopathologic subtypes. These heterogeneous histologic phenotypes originate from tumor cells with the distinct functions of tumorigenesis and self-renewal, called glioma stem cells (GSCs). GSCs are characterized based on multi-layered epigenetic mechanisms, which control the expression of many genes. This epigenetic regulatory mechanism is often based on functional non-coding RNAs (ncRNAs). ncRNAs have become increasingly important in the pathogenesis of human cancer and work as oncogenes or tumor suppressors to regulate carcinogenesis and progression. These RNAs by being involved in chromatin remodeling and modification, transcriptional regulation, and alternative splicing of pre-mRNA, as well as mRNA stability and protein translation, play a key role in tumor development and progression. Numerous studies have been performed to try to understand the dysregulation pattern of these ncRNAs in tumors and cancer stem cells (CSCs), which show robust differentiation and self-regeneration capacity. This review provides recent findings on the role of ncRNAs in glioma development and progression, particularly their effects on CSCs, thus accelerating the clinical implementation of ncRNAs as promising tumor biomarkers and therapeutic targets.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9593299 | PMC |
| http://dx.doi.org/10.1016/j.omto.2022.09.005 | DOI Listing |
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