ArticleOncotarget2016
Musashi-1 regulates AKT-derived IL-6 autocrinal/paracrinal malignancy and chemoresistance in glioblastoma.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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.
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
38 citing papers in PubMed, 53 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
- Integration of MRI radiomics with immune profiling to predict response to CDK6 inhibitors in high-grade glioma.Frontiers in immunology · 2026Observational
- Unmasking the potential: mechanisms of neuroinflammatory modulation by oncolytic viruses in glioblastoma.Exploration of targeted anti-tumor therapy · 2025Review
- Understanding the Immune System and Biospecimen-Based Response in Glioblastoma: A Practical Guide to Utilizing Signal Redundancy for Biomarker and Immune Signature Discovery.Current oncology (Toronto, Ont.) · 2024Review
- Hypoxia within the glioblastoma tumor microenvironment: a master saboteur of novel treatments.Frontiers in immunology · 2024Review
- RNA binding proteins in cancer chemotherapeutic drug resistance.Frontiers in cell and developmental biology · 2024Review
- Interleukin-6-controlled, mesenchymal stem cell-based sodium/iodide symporter gene therapy improves survival of glioblastoma-bearing mice.Molecular therapy oncolytics · 2023Article
- Strategic Decoy Peptides Interfere with MSI1/AGO2 Interaction to Elicit Tumor Suppression Effects.Cancers · 2022Article
- Review
- Correlation of IL-6 and JAK2/STAT3 signaling pathway with prognosis of nasopharyngeal carcinoma patients.Aging · 2021Article
- Musashi-1-A Stemness RBP for Cancer Therapy?Biology · 2021Review
- Musashi-1 Regulates MIF1-Mediated M2 Macrophage Polarization in Promoting Glioblastoma Progression.Cancers · 2021Article
- Article
- Review
- [A Review of Celluar Senescence and Tumor Treatment].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021Review
- Msi1 inhibits cervical cancer cell apoptosis by downregulating BAK through AKT signaling.Journal of Cancer · 2021Article
- Constitutive Musashi1 expression impairs mouse postnatal development and intestinal homeostasis.Molecular biology of the cell · 2021Article
- Musashi-1 promotes cancer stem cell properties of glioblastoma cells via upregulation of YTHDF1.Cancer cell international · 2020Article
- Is There Such a Thing as a Genuine Cancer Stem Cell Marker? Perspectives from the Gut, the Brain and the Dental Pulp.Biology · 2020Review
- Intracellular functions of RNA-binding protein, Musashi1, in stem and cancer cells.Stem cell research & therapy · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiform (GBM) is one of the most lethal human malignant brain tumors with high risks of recurrence and poor treatment outcomes. The RNA-binding protein Musashi-1 (MSI1) is a marker of neural stem/progenitor cells. Recent study showed that high expression level of MSI1 positively correlates with advanced grade of GBM, where MSI1 increases the growth of GBM. Herein, we explore the roles of MSI1 as well as the underlying mechanisms in the regulation of drug resistance and tumorigenesis of GBM cells. Our results demonstrated that overexpression of MSI1 effectively protected GBM cells from drug-induced apoptosis through down-regulating pro-apoptotic genes; whereas inhibition of AKT withdrew the MSI1-induced anti-apoptosis and cell survival. We further showed that MSI1 robustly promoted the secretion of the pro-inflammatory cytokine IL-6, which was governed by AKT activity. Autonomously, the secreted IL-6 enhanced AKT activity in an autocrine/paracrine manner, forming a positive feedback regulatory loop with the MSI1-AKT pathway. Our results conclusively demonstrated a novel drug resistance mechanism in GBM cells that MSI1 inhibits drug-induced apoptosis through AKT/IL6 regulatory circuit. MSI1 regulates both cellular signaling and tumor-microenvironmental cytokine secretion to create an intra- and intercellular niche for GBM to survive from chemo-drug attack.
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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.