ArticleNucleic acids research2018
Modulation of MKNK2 alternative splicing by splice-switching oligonucleotides as a novel approach for glioblastoma treatment.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 70 citations in OpenAlex.
- Deconvoluting the multi-faceted roles of alternative splicing events in cancer: From underlying mechanisms to innovative therapeutics.Acta pharmaceutica Sinica. B · 2026Review
- Immune-associated alternative splicing signatures define molecular subtypes in breast cancer.iScience · 2026Article
- Hsa_circ_0000313/miR-1224-3p/MKNK2 Axis Modulates CD4Mediators of inflammation · 2026Article
- Silencing serine/arginine-rich splicing factor 1 to induce apoptosis and autophagy-dependent cell death in cholangiocarcinoma through the correction of oncogenic splicing errors.Anatomy & cell biology · 2025Article
- NADScience advances · 2025Article
- Transcriptional Consequences of MeCP2 Knockdown and Overexpression in Mouse Primary Cortical Neurons.International journal of molecular sciences · 2025Article
- Deep indel mutagenesis reveals the regulatory and modulatory architecture of alternative exon splicing.Nature communications · 2025Article
- The emerging roles of aberrant alternative splicing in glioma.Cell death discovery · 2025Review
- Targeting RNA splicing modulation: new perspectives for anticancer strategy?Journal of experimental & clinical cancer research : CR · 2025Review
- Identifying Strong Neoantigen MHC-I/II Binding Candidates for Targeted Immunotherapy with SINE.International journal of molecular sciences · 2024Article
- Steering research on mRNA splicing in cancer towards clinical translation.Nature reviews. Cancer · 2024Review
- Nucleic acid drugs: recent progress and future perspectives.Signal transduction and targeted therapy · 2024Review
- Protein isoform-centric therapeutics: expanding targets and increasing specificity.Nature reviews. Drug discovery · 2024Review
- A-Z of Epigenetic Readers: Targeting Alternative Splicing and Histone Modification Variants in Cancer.Cancers · 2024Review
- Circular RNA AGAP1 Stimulates Immune Escape and Distant Metastasis in Renal Cell Carcinoma.Molecular biotechnology · 2024Article
- Modification of BCLX pre-mRNA splicing has antitumor efficacy alone or in combination with radiotherapy in human glioblastoma cells.Cell death & disease · 2024Article
- Alternative splicing and related RNA binding proteins in human health and disease.Signal transduction and targeted therapy · 2024Review
- MiR-125b targeted regulation of MKNK2 inhibits multiple myeloma proliferation and invasion.American journal of translational research · 2024Article
- Article
- Therapeutic Targeting of RNA Splicing in Cancer.Genes · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The gene encoding the kinase Mnk2 (MKNK2) is alternatively spliced to produce two isoforms-Mnk2a and Mnk2b. We previously showed that Mnk2a is downregulated in several types of cancer and acts as a tumor suppressor by activation of the p38-MAPK stress pathway, inducing apoptosis. Moreover, Mnk2a overexpression suppressed Ras-induced transformation in culture and in vivo. In contrast, the Mnk2b isoform acts as a pro-oncogenic factor. In this study, we designed modified-RNA antisense oligonucleotides and screened for those that specifically induce a strong switch in alternative splicing of the MKNK2 gene (splice switching oligonucleotides or SSOs), elevating the tumor suppressive isoform Mnk2a at the expense of the pro-oncogenic isoform Mnk2b. Induction of Mnk2a by SSOs in glioblastoma cells activated the p38-MAPK pathway, inhibited the oncogenic properties of the cells, re-sensitized the cells to chemotherapy and inhibited glioblastoma development in vivo. Moreover, inhibition of p38-MAPK partially rescued glioblastoma cells suggesting that most of the anti-oncogenic activity of the SSO is mediated by activation of this pathway. These results suggest that manipulation of MKNK2 alternative splicing by SSOs is a novel approach to inhibit glioblastoma tumorigenesis.
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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.