ArticleJournal of cancer research and clinical oncology2024
AKT1-Mediated NOTCH1 phosphorylation promotes gastric cancer progression via targeted regulation of IRS-1 transcription.
Article in Journal of cancer research and clinical oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed.
- Targeting the akt/mtor signaling pathway by maprotiline leads to tumor suppression in T-cell lymphoma.Annals of hematology · 2025Article
- TRIM32 promotes tumor immune evasion and impedes Anti-PD-1 treatment by inducing immunosuppressive macrophages in gastric cancer.Journal of translational medicine · 2025Article
- Mechanism of 15-hydroxyprostaglandin dehydrogenase protein inhibiting cervical cancer cell proliferation through downregulation of the notch1 signaling pathway.CytoJournal · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
purposeThis study aimed to investigate that AKT1-Mediated NOTCH1 phosphorylation promotes gastric cancer (GC) progression via targeted regulation of IRS-1 transcription.
methodsThe study utilized databases such as PhosphositePlus, TRANSFAC, CHEA, GPS 5.0, and TCGA, along with experimental techniques including Western Blot, co-IP, in vitro kinase assay, construction of lentiviral overexpression and silencing vectors, immunoprecipitation, modified proteomics, immunofluorescence, ChIP-PCR, EdU assay, Transwell assay, and scratch assay to investigate the effects of AKT1-induced Notch1 phosphorylation on cell proliferation, invasion and migration in vitro, as well as growth and epithelial-mesenchymal transition (EMT) in vivo.
resultsAKT1 was found to induce phosphorylation of Notch1 at the S2183 site in GC, subsequently altering the subcellular localization of Notch1-IC and promoting its nuclear translocation. The transcription factor RBPJ that binds to Notch1 transcriptionally regulated IRS-1, CDH5, TNL1, ASCL2, and LRP6. Experimental validation revealed that Notch1-IC can regulate the expression of IRS-1. Overexpression of Notch1-IC was shown to promote the proliferation, invasion, and metastasis of GC cells, while knockdown of IRS-1 partially inhibited the aforementioned effects induced by Notch1-IC overexpression. Further experiments in vitro and vivo confirmed that AKT1-induced Notch1 phosphorylation can regulate the expression of IRS-1 and promote the malignant behavior of GC, including proliferation, invasion, metastasis, and EMT, with knockdown of IRS-1 partially reversing these effects.
conclusionAKT1 induces the Notch1 phosphorylation and promotes the activation and nuclear translocation of Notch1-IC by targeting the regulation of IRS-1, thereby advancing the progression of GC.
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Registered trials
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