ArticleCell death & disease2019
Alternative splicing-derived intersectin1-L and intersectin1-S exert opposite function in glioma progression.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- OY-TES-1 Splice Variant V5a in Glioma: A Driver of Malignancy and Potential Therapeutic Target.Current medical science · 2026Article
- mRNA processing in cancer immunotherapy: emerging targets, resistance mechanisms, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Alternative splicing of bunched confers a dual role in hippo pathway-dependent growth and tumorigenesis.Oncogene · 2025Article
- The emerging roles of aberrant alternative splicing in glioma.Cell death discovery · 2025Review
- Article
- Development and validation of a prognostic model based on RNA binding proteins in patients with esophageal cancer.Journal of thoracic disease · 2023Article
- The alternative splicing of intersectin 1 regulated by PTBP1 promotes human glioma progression.Cell death & disease · 2022Article
- EventPointer 3.0: flexible and accurate splicing analysis that includes studying the differential usage of protein-domains.NAR genomics and bioinformatics · 2022Article
- LINC00941 promotes pancreatic cancer malignancy by interacting with ANXA2 and suppressing NEDD4L-mediated degradation of ANXA2.Cell death & disease · 2022Article
- Development and validation of novel prognostic models based on RNA-binding proteins in breast cancer.The Journal of international medical research · 2022Article
- Landscape of Alternative Splicing Events Related to Prognosis and Immune Infiltration in Glioma: A Data Analysis and Basic Verification.Journal of immunology research · 2022Article
- Endocytic protein intersectin1-S shuttles into nucleus to suppress the DNA replication in breast cancer.Cell death & disease · 2021Article
- MYC-mediated upregulation of PNO1 promotes glioma tumorigenesis by activating THBS1/FAK/Akt signaling.Cell death & disease · 2021Article
- Aquaporin 1 promotes sensitivity of anthracycline chemotherapy in breast cancer by inhibiting β-catenin degradation to enhance TopoIIα activity.Cell death and differentiation · 2021Article
- Prognostic Value and Biological Functions of RNA Binding Proteins in Stomach Adenocarcinoma.OncoTargets and therapy · 2021Article
- Signature of gene aberrant alternative splicing events in pancreatic adenocarcinoma prognosis.Journal of Cancer · 2021Article
- Systematic Analysis of Survival-Associated Alternative Splicing Signatures in Thyroid Carcinoma.Frontiers in oncology · 2021Article
- Integrated analysis of the roles and prognostic value of RNA binding proteins in lung adenocarcinoma.PeerJ · 2020Article
- Review
- Identification of TUBB4A as a Prognostic Biomarker of Melanoma by Transcriptomic Data andTechnology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intersectin1 (ITSN1) contains two isoforms: ITSN1-S and ITSN1-L, which is highly regulated by alternative splicing. However, the alteration of alternative splicing and its importance in cancer is still unknown. In this study, our transcriptome analysis by using a large glioma cohort indicated the two isoforms exerted opposite function in glioma progression. Our previous results had shown ITSN1-S could promote glioma development; however, the function of ITSN1-L remained unknown. In this study, we first confirmed that ITSN1-L exerted an inhibitory role in glioma progression both in vivo and in vitro, which was contrary to the function of ITSN1-S. In additional, we also elucidated the mechanisms of ITSN1-L in inhibiting tumor progression. First, we revealed ITSN1-L could interact with α-tubulin to promote HDAC6-dependent deacetylation of ac-tubulin leading to decreased cell motility. Second, ITSN1-L could attenuate cell-substrate adhesion through FAK/integrin β3 pathway. Third, ITSN1-L was able to strengthen cell-cell adhesion by upregulating N-cadherin expression and its re-localization to membrane by ANXA2 and TUBB3/TUBB4. In conclusion, we found for the first time that two isoforms produced by alternative splicing exerted opposite functions in glioma development. Therefore, upregulation of ITSN1-L expression as well as downregulation of ITSN1-S expression probably was a better strategy in glioma treatment. Our present study laid a foundation for the importance of alternative splicing in glioma progression and raised the possibility of controlling glioma development completely at an alternative splicing level to be a more effective strategy.
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