ArticleCancer cell international2020
Musashi-1 promotes cancer stem cell properties of glioblastoma cells via upregulation of YTHDF1.
Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- mRNA markers for survival prediction in glioblastoma multiforme patients: a systematic review with bioinformatic analyses.BMC cancer · 2024Pooled it
- Musashi-1 Drives Radioresistance and Stemness in Head and Neck Squamous Cell Carcinoma via a Radioresistant FaDu Model.Cancer science · 2026Article
- RNA modifications as determinants of cancer cell death: from epitranscriptomic mechanisms to therapeutic targeting.Functional & integrative genomics · 2026Review
- Computational design and immunoinformatics validation of a T cell multi-epitope vaccine targeting glioblastoma stem cells.Scientific reports · 2026Article
- Tumor heterogeneity and resistance in glioblastoma: the role of stem cells.Apoptosis : an international journal on programmed cell death · 2025Review
- Loss of Epitranscriptomic Modification NTranslational stroke research · 2025Article
- Musashi-dependent mRNA translational activation is mediated through association with the Scd6/Like-sm family member, LSM14B.Scientific reports · 2025Article
- The role of N(6)-methyladenosine (m6a) modification in cancer: recent advances and future directions.EXCLI journal · 2025Review
- The role of RNA methylation in glioma progression: mechanisms, diagnostic implications, and therapeutic value.Frontiers in immunology · 2025Review
- Pan-cancer analysis of COL15A1: an immunological and prognostic biomarker.Discover oncology · 2024Article
- Cancer stem cells: advances in knowledge and implications for cancer therapy.Signal transduction and targeted therapy · 2024Review
- Deciphering the role of transcription factors in glioblastoma cancer stem cells.Acta biochimica et biophysica Sinica · 2024Review
- Small molecule inhibitors targeting mJournal of hematology & oncology · 2024Review
- YTHDF1 promotes the viability and self‑renewal of glioma stem cells by enhancing LINC00900 stability.International journal of oncology · 2024Article
- Role of N6-methyladenosine methylation in glioma: recent insights and future directions.Cellular & molecular biology letters · 2023Review
- The effects of NMolecular and cellular biochemistry · 2023Review
- Insights into the regulatory role of RNA methylation modifications in glioma.Journal of translational medicine · 2023Review
- m6A-TSHub: Unveiling the Context-specific mGenomics, proteomics & bioinformatics · 2023Article
- Review
- The Regulation of m6A Modification in Glioblastoma: Functional Mechanisms and Therapeutic Approaches.Cancers · 2023Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundGlioblastoma (GBM) is the most lethal brain tumor characterized by high morbidity and limited treatment options. Tumor malignancy is usually associated with the epigenetic marks, which coordinate gene expression to ascertain relevant phenotypes. One of such marks is m6A modification of RNA, whose functional effects are dependent on the YTH family m6A reader proteins. METHODS AND
resultsIn this study, we investigated the expression of five YTH family proteins in different GBM microarray datasets from the Oncomine database, and identified YTHDF1 as the most highly overexpressed member of this family in GBM. By performing the knockdown of YTHDF1 in a GBM cell line, we found that it positively regulates proliferation, chemoresistance and cancer stem cell-like properties. Musashi-1 (MSI1) is a postranscriptional gene expression regulator associated with high oncogenicity in GBM. By knocking down and overexpressing MSI1, we found that it positively regulates YTHDF1 expression. The inhibitory effects imposed on the processes of proliferation and migration by YTHDF1 knockdown were shown to be partially rescued by concomitant overexpression of MSI1. MSI1 and YTHDF1 were shown to be positively correlated in clinical glioma samples, and their concomitant upregulation was associated with decreased survival of glioma patients. We identified the direct regulation of YTHDF1 by MSI1.
conclusionsGiven the fact that both proteins are master regulators of gene expression, and both of them are unfavorable factors in GBM, we suggest that in any future studies aimed to uncover the prognostic value and therapy potential, these two proteins should be considered together.
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