ArticleNature communications2016
Inhibition of Notch pathway arrests PTEN-deficient advanced prostate cancer by triggering p27-driven cellular senescence.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 48 citations in OpenAlex.
- Review
- Article
- Kaempferol triggers cellular senescence via CDK1 ubiquitination in HCC cells.Cancer cell international · 2025Article
- NOTCH1 inhibition enhances immunogenicity and sensitizes triple-negative breast cancer to immune checkpoint inhibitors.Breast cancer research : BCR · 2025Article
- Identification of CCNB1 as a biomarker for cellular senescence in hepatocellular carcinoma: a bioinformatics and experimental validation study.Discover oncology · 2025Article
- Notch signaling pathway in cancer: from mechanistic insights to targeted therapies.Signal transduction and targeted therapy · 2024Review
- Article
- Therapeutic role of PTEN in tissue regeneration for management of neurological disorders: stem cell behaviors to an in-depth review.Cell death & disease · 2024Review
- Aberrant activated Notch1 promotes prostate enlargement driven by androgen signaling via disrupting mitochondrial function in mouse.Cellular and molecular life sciences : CMLS · 2024Article
- Regulation of EZH2 Expression by INPP4B in Normal Prostate and Primary Prostate Cancer.Cancers · 2023Article
- Knocking down SOX2 overcomes the resistance of prostate cancer to castration via notch signaling.Molecular biology reports · 2023Article
- The roles of proteases in prostate cancer.IUBMB life · 2023Review
- ARPC5 is transcriptionally activated by KLF4, and promotes cell migration and invasion in prostate cancer via up-regulating ADAM17 : ARPC5 serves as an oncogene in prostate cancer.Apoptosis : an international journal on programmed cell death · 2023Article
- Article
- PTEN Protein Phosphatase Activity Is Not Required for Tumour Suppression in the Mouse Prostate.Biomolecules · 2022Article
- Interplay of Developmental Hippo-Notch Signaling Pathways with the DNA Damage Response in Prostate Cancer.Cells · 2022Review
- SOX8 Knockdown Overcomes Enzalutamide Resistance in Castration-Resistant Prostate Cancer by Inhibiting the Notch Signaling Pathway.BioMed research international · 2022Article
- HER3 Is an Actionable Target in Advanced Prostate Cancer.Cancer research · 2021Article
- Transcription factor network analysis based on single cell RNA-seq identifies that Trichostatin-a reverses docetaxel resistance in prostate Cancer.BMC cancer · 2021Article
- Palbociclib induces cell senescence and apoptosis of gastric cancer cells by inhibiting the Notch pathway.Oncology letters · 2021Article
Corrections and comments
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Authors and funding
19 authors at 6 institutions in 4 countries.
Funding
Abstract
Activation of NOTCH signalling is associated with advanced prostate cancer and treatment resistance in prostate cancer patients. However, the mechanism that drives NOTCH activation in prostate cancer remains still elusive. Moreover, preclinical evidence of the therapeutic efficacy of NOTCH inhibitors in prostate cancer is lacking. Here, we provide evidence that PTEN loss in prostate tumours upregulates the expression of ADAM17, thereby activating NOTCH signalling. Using prostate conditional inactivation of both Pten and Notch1 along with preclinical trials carried out in Pten-null prostate conditional mouse models, we demonstrate that Pten-deficient prostate tumours are addicted to the NOTCH signalling. Importantly, we find that pharmacological inhibition of γ-secretase promotes growth arrest in both Pten-null and Pten/Trp53-null prostate tumours by triggering cellular senescence. Altogether, our findings describe a novel pro-tumorigenic network that links PTEN loss to ADAM17 and NOTCH signalling, thus providing the rational for the use of γ-secretase inhibitors in advanced prostate cancer patients.
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Registered trials
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.