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    GENE:

    MSI2 (Musashi RNA Binding Protein 2)

    i
    Other names: MSI2, Musashi RNA Binding Protein 2, RNA-Binding Protein Musashi Homolog 2, Musashi-2, Musashi Homolog 2 (Drosophila), Musashi Homolog 2, MSI2H
    17d
    Systematic functional dissection of germline noncoding risk variants impacting clonal hematopoiesis. (PubMed, bioRxiv)
    We used targeted genome editing to demonstrate endogenous enhancer activity across 3 MPRA variants that affect the transcription of NKD2, FLT3, and MSI2. Our functional studies on MSI2 indicate that presence of higher levels of MSI2 mediated by CHIP risk allele enhances the clonal expansion of TET2 knockout hematopoietic stem and progenitor cells, providing a mechanistic link whereby non-coding genetic variants can influence the expansion of mutant CHIP clones.
    Journal
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    FLT3 (Fms-related tyrosine kinase 3) • TET2 (Tet Methylcytosine Dioxygenase 2) • CD34 (CD34 molecule) • MSI2 (Musashi RNA Binding Protein 2)
    28d
    The RNA-Binding Protein MSI2 Controls Blood-Tumor Barrier Permeability via LINC00667-Mediated IRF6 mRNA Decay. (PubMed, J Biol Chem)
    Furthermore, both individual and combined modulation of MSI2 knockdown, LINC00667 knockdown and IRF6 over-expression enhanced BTB permeability to doxorubicin (Dox), thereby increasing the apoptosis rate of GB cells. Collectively, the MSI2/LINC00667/IRF6 pathway plays an important role in modulating BTB permeability, offering potential targets for new molecular therapies in GB.
    Journal
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    MSI2 (Musashi RNA Binding Protein 2) • TJP1 (Tight Junction Protein 1) • CLDN5 (Claudin 5) • IRF6 (Interferon Regulatory Factor 6) • LINC00667 (Long Intergenic Non-Protein Coding RNA 667) • OCLN (Occludin)
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    doxorubicin hydrochloride
    2ms
    Identification of a Musashi2 translocation as a novel oncogene in myeloid leukemia. (PubMed, Elife)
    Although Gleevec has been transformative for CML, blast crisis CML remains relatively drug resistant...These data suggest that MSI2-HOXA9 acts, at least in part, by increasing expression of the mitochondrial polymerase POLRMT and augmenting mitochondrial function and basal respiration in blast crisis. Collectively, our findings demonstrate for the first time that translocations involving the stem and developmental signal MSI2 can be oncogenic and suggest that MSI, which we found to be a frequent partner for an array of translocations, could also be a driver mutation across solid cancers.
    Journal
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    ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • HOXA9 (Homeobox A9) • RRM1 (Ribonucleotide Reductase Catalytic Subunit M1) • RRM2 (Ribonucleotide Reductase Regulatory Subunit M2) • MSI2 (Musashi RNA Binding Protein 2)
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    imatinib
    2ms
    Inherited resilience to clonal hematopoiesis by modifying stem cell RNA regulation. (PubMed, Science)
    Variant rs17834140-T was associated with slower CH expansion, and stem cell MSI2 levels modified ASXL1-mutant HSC clonal dominance. These findings leverage natural resilience to illuminate posttranscriptional regulation in human HSCs, suggesting that inhibition of MSI2 or its targets could be rational strategies for blood cancer prevention.
    Journal
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    ASXL1 (ASXL Transcriptional Regulator 1) • MSI2 (Musashi RNA Binding Protein 2)
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    ASXL1 mutation
    3ms
    MSI2 exerts antitumor effects by regulating T-cell function in kidney renal clear cell carcinoma. (PubMed, Transl Androl Urol)
    Our results suggest that MSI2 plays an antitumor role in KIRC by regulating T-cell function. They also indicate that MSI2 is involved in hydrogen ion secretion in renal tubular epithelial cells and that it may be a differentiation and maturation marker in these cells.
    Journal
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    MSI2 (Musashi RNA Binding Protein 2)
    3ms
    Targeting Musashi-2 to counteract senescence and resistance in chronic myeloid leukemia: enhancing the efficacy of imatinib therapy. (PubMed, BMC Cancer)
    In conclusion, MSI2 inhibition, in combination with TKI therapy, has shown to overcome drug resistance and mitigate senescence in preclinical CML models, and suggesting a potential strategy to target CML LSCs.
    Journal
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    ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • IL6 (Interleukin 6) • HIF1A (Hypoxia inducible factor 1, alpha subunit) • CDKN1A (Cyclin-dependent kinase inhibitor 1A) • MSI2 (Musashi RNA Binding Protein 2)
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    imatinib
    3ms
    Genomic and Demographic Characteristics of Angiosarcoma as Described in the AACR Project GENIE Registry. (PubMed, Cancers (Basel))
    In one of the largest genomic analyses of angiosarcoma to date, we identified recurrent alterations, suggesting potential future therapeutic targets.
    Journal
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    TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • FGFR1 (Fibroblast growth factor receptor 1) • NTRK2 (Neurotrophic tyrosine kinase, receptor, type 2) • HRAS (Harvey rat sarcoma viral oncogene homolog) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • ARID1A (AT-rich interaction domain 1A) • NOTCH1 (Notch 1) • KDR (Kinase insert domain receptor) • MTAP (Methylthioadenosine Phosphorylase) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) • ATRX (ATRX Chromatin Remodeler) • NOTCH2 (Notch 2) • FAT1 (FAT atypical cadherin 1) • FLT4 (Fms-related tyrosine kinase 4) • CRKL (CRK Like Proto-Oncogene, Adaptor Protein) • POT1 (Protection of telomeres 1) • MSI2 (Musashi RNA Binding Protein 2) • ZFHX4 (Zinc Finger Homeobox 4)
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    TP53 mutation • PIK3CA mutation • CDKN2A deletion
    3ms
    Potential signaling pathways, biomarkers, natural drugs, and chronic myeloid leukemia therapeutics. (PubMed, Front Pharmacol)
    Tyrosine kinase inhibitors like imatinib can kill and eradicate BCR-ABL1 translocated cells, but they cannot directly target BCR-ABL1 leukemia stem cells...There are handful number of proteins such as Musashi2 which have substantial diagnostic use in leukemia treatment and strategy. After going through a number recent develeopments in CML and its therapeutics, I presented here an overview of the latest advancements in CML, natural drugs, biomarkers, potential signaling pathways, and treatment strategies.
    Review • Journal
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    ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • MSI2 (Musashi RNA Binding Protein 2)
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    imatinib
    5ms
    CircNR3C1 Promotes Acute Lymphoblastic Leukemia Progression via the MSI2/ENO1/RPS3 Axis. (PubMed, J Leukoc Biol)
    These findings indicate that circNR3C1 promotes ALL cell proliferation and inhibits apoptosis by interacting with MSI2 to stabilize ENO1 mRNA, leading to upregulation of ENO1 and RPS3. The circNR3C1/MSI2/ENO1/RPS3 axis represents a novel regulatory pathway contributing to ALL progression and offers potential therapeutic targets for treatment.
    Journal
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    ENO1 (Enolase 1) • MSI2 (Musashi RNA Binding Protein 2) • NR3C1 (Nuclear Receptor Subfamily 3 Group C Member 1)
    5ms
    A Circular RNA Promotes Tumor Metastasis through Stabilizing MSI2 Protein in Pancreatic Ductal Adenocarcinoma. (PubMed, Research (Wash D C))
    Notably, we validated the translational potential of circPRKD3 as a liquid biopsy marker, showing that serum detection, when combined with conventional biomarkers (CA19-9, CEA, and CA125), dramatically improved diagnostic performance. These findings not only delineate a novel circRNA-mediated regulatory axis in PDAC metastasis but also identify circPRKD3 as a promising diagnostic and prognostic biomarker.
    Journal
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    MUC16 (Mucin 16, Cell Surface Associated) • MSI2 (Musashi RNA Binding Protein 2) • CA 19-9 (Cancer antigen 19-9)
    5ms
    Regulation of metabolic adaptation and leukemia progression by MUSASHI2-DEPTOR-KIF11 axis. (PubMed, Leukemia)
    Mechanistically, DEPTOR stabilizes KIF11 by preventing its ubiquitination and proteasomal degradation, thereby ensuring proper mTORC1 localization and metabolic adaptation during nutrient stress. Collectively, our findings establish the MSI2/DEPTOR/KIF11 axis as a critical driver of leukemogenesis and a promising therapeutic target for aggressive myeloid leukemias.
    Journal
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    ATF4 (Activating Transcription Factor 4) • KIF11 (Kinesin Family Member 11) • MSI2 (Musashi RNA Binding Protein 2)