ArticleMolecular medicine (Cambridge, Mass.)2021
Phosphorylation of islet-1 serine 269 by CDK1 increases its transcriptional activity and promotes cell proliferation in gastric cancer.
Article in Molecular medicine (Cambridge, Mass.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 16 citations in OpenAlex.
- A Prognostic Risk Model Based on Immune Genes in Thyroid Cancer and Its Correlation With Tumor-Associated Immune Cell Infiltration Abundance.Cancer medicine · 2026Article
- Decoding the PTM code of cGAS-STING in gastric cancer: from innate DNA sensing to precision combination therapy.Frontiers in immunology · 2026Review
- Landscape analysis of m5C modification regulators unveils DNMT1-mediated dysregulated pyrimidine metabolism in hepatocellular carcinoma.Clinical epigenetics · 2025Article
- Structural basis of phosphorylation-independent nuclear import of CIRBP by TNPO3.Nature communications · 2025Article
- Post translational modification regulation of transcription factors governing pancreatic β-cell identity and functional mass.Frontiers in endocrinology · 2025Review
- EphrinB2-mediated CDK5/ISL1 pathway enhances cardiac lymphangiogenesis and alleviates ischemic injury by resolving post-MI inflammation.Signal transduction and targeted therapy · 2024Article
- Exploration of the link between COVID-19 and gastric cancer from the perspective of bioinformatics and systems biology.Frontiers in medicine · 2024Article
- Targeting CDK1 in cancer: mechanisms and implications.NPJ precision oncology · 2023Review
- Epigenetic and Tumor Microenvironment for Prognosis of Patients with Gastric Cancer.Biomolecules · 2023Article
- Identification and characterization of the CDK1-BMAL1-UHRF1 pathway driving tumor progression.iScience · 2023Article
- The Regulation of Cyclins and Cyclin-Dependent Kinases in the Development of Gastric Cancer.International journal of molecular sciences · 2023Review
- A review on the role of cyclin dependent kinases in cancers.Cancer cell international · 2022Review
- Dihydroartemisinin Suppresses the Tumorigenesis and Cycle Progression of Colorectal Cancer by Targeting CDK1/CCNB1/PLK1 Signaling.Frontiers in oncology · 2021Article
- CDK10 in Gastrointestinal Cancers: Dual Roles as a Tumor Suppressor and Oncogene.Frontiers in oncology · 2021Review
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDespite recent advances in diagnostic and therapeutic approaches for gastric cancer (GC), the survival of patients with advanced GC remains very low. Islet-1 (ISL1) is a LIM-homeodomain transcription factor, which is upregulated and promotes cell proliferation in GC. The exact mechanism by which ISL1 influences GC development is unclear.
methodsCo-immunoprecipitation (co-IP) and glutathione S-transferase (GST)-pulldown assays were employed to evaluate the interaction of ISL1 with CDK1. Western blot and immunohistochemistry analyses were performed to evaluate the ability of CDK1 to phosphorylate ISL1 at Ser 269 in GC cell and tissue specimens. Chromatin immunoprecipitation (ChIP), ChIP re-IP, luciferase reporter, and CCK-8 assays were combined with flow cytometry cell cycle analysis to detect the transactivation potency of ISL1-S269-p and its ability to promote cell proliferation. The self-stability and interaction with CDK1 of ISL1-S269-p were also determined.
resultsISL1 is phosphorylated by CDK1 at serine 269 (S269) in vivo. Phosphorylation of ISL1 by CDK1 on serine 269 strengthened its binding on the cyclin B1 and cyclin B2 promoters and increased its transcriptional activity in GC. Furthermore, CDK1-dependent phosphorylation of ISL1 correlated positively with ISL1 protein self-stability in NIH3T3 cells.
conclusionsISL1-S269-p increased ISL1 transcriptional activity and self-stability while binding to the cyclinB1 and cyclinB2 promoters promotes cell proliferation. ISL1-S269-p is therefore crucial for tumorigenesis and potentially a direct therapeutic target for GC.
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