ArticleThe Journal of biological chemistry2009
Zinc finger transcription factor INSM1 interrupts cyclin D1 and CDK4 binding and induces cell cycle arrest.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 50 citations in OpenAlex.
- Article
- High-throughput investigation of cyclin docking interactions reveals the complexity of motif binding determinants.Nature communications · 2025Article
- A Trade-Off between Body Mass and Cancer Resistance in Cetaceans Is Mediated by Cell Cycle-Related Gene Evolution.Molecular biology and evolution · 2025Article
- Structural insights into a highly flexible zinc finger module unravel INSM1 function in transcription regulation.Nature communications · 2025Article
- An innovative prognostic auxiliary for colon adenocarcinoma based on zinc finger protein genes.Translational cancer research · 2024Article
- Regulation of Molecular Biomarkers Associated with the Progression of Prostate Cancer.International journal of molecular sciences · 2024Review
- Repurposing a plant alkaloid homoharringtonine targets insulinoma associated-1 in N-Myc-activated neuroblastoma.Cellular signalling · 2023Article
- [Expression and significance of INSM1 and SOX11 in pancreatic neuroendocrine tumor and solid pseudopapillary neoplasm].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2023Article
- Review
- INSM1 Expression in Mesenchymal Tumors and Its Clinicopathological Significance.BioMed research international · 2022Article
- A miR-375/YAP axis regulates neuroendocrine differentiation and tumorigenesis in lung carcinoid cells.Scientific reports · 2021Article
- Transcriptomic analysis identifies a tumor subtype mRNA classifier for invasive non-functioning pituitary neuroendocrine tumor diagnostics.Theranostics · 2021Article
- Identification of a MicroRNA Signature Associated With Lymph Node Metastasis in Endometrial Endometrioid Cancer.Frontiers in genetics · 2021Article
- A promoter-driven assay for INSM1-associated signaling pathway in neuroblastoma.Cellular signalling · 2020Article
- Insulinoma-associated protein 1 (INSM1): a potential biomarker and therapeutic target for neuroendocrine tumors.Cellular oncology (Dordrecht, Netherlands) · 2020Review
- Insulinoma-Associated-1: From Neuroendocrine Tumor Marker to Cancer Therapeutics.Molecular cancer research : MCR · 2019Review
- let-7 MicroRNA-Mediated Regulation of Shh Signaling and the Gene Regulatory Network Is Essential for Retina Regeneration.Cell reports · 2018Article
- Overexpression of the proneural transcription factor ASCL1 in chronic lymphocytic leukemia with a t(12;14)(q23.2;q32.3).Molecular cytogenetics · 2018Article
- REST corepressors RCOR1 and RCOR2 and the repressor INSM1 regulate the proliferation-differentiation balance in the developing brain.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
INSM1 is a zinc finger transcription factor that plays an important role in pancreatic beta-cell development. To further evaluate its role in cell fate determination, we investigated INSM1 effects on cell cycle function. The cyclin box of cyclin D1 is essential for INSM1 binding. Competitive pull-down and co-immunoprecipitation revealed that INSM1 binding to cyclin D1 interrupts its association with CDK4 and induces hypophosphorylation of the retinoblastoma protein. An inducible Tet-on system was established in Cos-7 and Panc-1 cells. Using serum starvation, we synchronized the cell cycle and subsequently induced cell cycle progression by serum stimulation. Comparison of the INSM1 induction group with the noninduced control group, INSM1 ectopic expression causes cell cycle arrest, whereas the INSM1-mediated cell cycle arrest could be reversed by cyclin D1 and CDK4 overexpression. The proline-rich N-terminal portion of INSM1 is required for cyclin D1 binding. Mutation of proline residues abolished cyclin D1 binding and also diminished its ability to induce cell cycle arrest. Cellular proliferation of Panc-1 cells was inhibited by INSM1 overexpression demonstrated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, soft agar colony formation, as well as tumor growth in a nude mouse model. Taken together, we provide evidence to support that INSM1 binds to cyclin D1, interrupts cell cycle signaling, and inhibits cellular proliferation.
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