ArticleNeoplasia (New York, N.Y.)2019
Musashi-1 Enhances Glioblastoma Migration by Promoting ICAM1 Translation.
Article in Neoplasia (New York, N.Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 46 citations in OpenAlex.
- Clinicopathological significance and prognostic value of the MSI1/MTFR2 axis in clear cell renal cell carcinoma: linking stemness and mitochondrial dynamics.Medical molecular morphology · 2026Article
- Inhibition of ICAM1 diminishes stemness and enhances antitumor immunity in glioblastoma via β-catenin/PD-L1 signaling.Nature communications · 2025Article
- Identifying survival subtypes with autoencoder using multiple types of high-dimensional genomic data from studies of glioblastoma multiforme.Briefings in bioinformatics · 2025Article
- Expression of stem cell marker musashi-1 and its relationship with survival prognosis in patients with resectable esophageal squamous cell carcinoma.World journal of stem cells · 2025Article
- Tumor heterogeneity and resistance in glioblastoma: the role of stem cells.Apoptosis : an international journal on programmed cell death · 2025Review
- Regulatory Effects of RNA-Protein Interactions Revealed by Reporter Assays of Bacteria Grown on Solid Media.Biosensors · 2025Article
- Systematic Analysis of an Immune-Related Gene Signature for Predicting Prognosis and Immune Characteristics in Primary Lower Grade Glioma.BioMed research international · 2025Article
- Immunosuppressive Microenvironment in H3K27 Mutant Pediatric Diffuse Midline Glioma: Single-Cell and Bioinformatics Insights on CD8A, IL7R, and ICAM1.Current medicinal chemistry · 2025Article
- Role of adhesion molecules in cancer and targeted therapy.Science China. Life sciences · 2024Review
- Exosomal Circ_FMN2 Derived from the Serum of Colorectal Cancer Patients Promotes Cancer Progression by miR-338-3p/MSI1 Axis.Applied biochemistry and biotechnology · 2023Article
- Musashi-1 regulates cell cycle and confers resistance to cisplatin treatment in Group 3/4 medulloblastomas cells.Human cell · 2023Article
- Roles of STAT3 in the pathogenesis and treatment of glioblastoma.Frontiers in cell and developmental biology · 2023Review
- Genome-Wide Association Study Identifies Multiple Susceptibility Loci for Malignant Neoplasms of the Brain in Taiwan.Journal of personalized medicine · 2022Article
- Knockdown of the stem cell marker Musashi-1 inhibits endometrial cancer growth and sensitizes cells to radiation.Stem cell research & therapy · 2022Article
- Tumour-associated CD204Neuropathology and applied neurobiology · 2022Article
- Comprehensive analysis of prognosis-related alternative splicing events in ovarian cancer.RNA biology · 2022Article
- Overview of the molecular mechanisms of migration and invasion in glioblastoma multiforme.Journal of the Chinese Medical Association : JCMA · 2021Article
- Musashi-1-A Stemness RBP for Cancer Therapy?Biology · 2021Review
- Increased expression of MUSASHI1 in epithelial breast cancer cells is due to down regulation of miR-125b.BMC molecular and cell biology · 2021Article
- A System Bioinformatics Approach Predicts the Molecular Mechanism Underlying the Course of Action of Radix Salviae Reverses GBM Effects.Evidence-based complementary and alternative medicine : eCAM · 2021Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is a lethal brain tumor with a mean survival time of 1 year. One major reason for therapeutic failure is that GBM cells have an extraordinary capacity to invade normal brain tissue beyond the surgical margin, accounting for the lack of treatment efficacy. GBM cells that can infiltrate into the healthy brain possess tumor properties of stemness and invasion, and previous studies demonstrate that Musashi-1 (MSI1), a neural stem cell marker, plays an important role in the maintenance of stem cell status, cellular differentiation, and tumorigenesis in cancers. By analyzing neuronal progenitor cell markers and stemness genes, we predicted that MSI1 might be an important factor in GBM pathogenesis. Because inflammation aids in the proliferation and survival of malignant cells, the inflammatory microenvironment also promotes GBM invasion, and intercellular adhesion molecule-1 (ICAM1), a member of the immunoglobulin superfamily, is involved in inflammation. Our results indicate that the above phenomena are likely due to MSI1 upregulation, which occurred simultaneously with higher expression of ICAM1 in GBM cells. Indeed, MSI1 knockdown effectively suppressed ICAM1 expression and blocked GBM cell motility and invasion, whereas overexpressing ICAM1 reversed these effects. According to RNA immunoprecipitation assays, MSI1-mediated mRNA interactions promote ICAM1 translation. Finally, immunohistochemical analysis showed MSI1 and ICAM-1 to be coexpressed at high levels in GBM tissues. Thus, the MSI1/ICAM1 pathway plays an important role in oncogenic resistance, including increased tumor invasion, and MSI1/ICAM1 may be a target for GBM treatment.
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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.