ArticleOncogene2016
Prolyl-isomerase Pin1 controls Notch3 protein expression and regulates T-ALL progression.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 53 citations in OpenAlex.
- PIN1 inhibits ferroptosis in gastric cancer cells by regulating the CPEB1‑GPX4 pathway.Oncology reports · 2026Article
- Prolyl-isomerase Pin1 drives platinum resistance by regulating Notch3 stability and function in ovarian cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- Modes of Notch signalling in development and disease.Nature reviews. Molecular cell biology · 2025Review
- A tethering mechanism underlies Pin1-catalyzed prolineProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Notch3-regulated microRNAs impair CXCR4-dependent maturation of thymocytes allowing maintenance and progression of T-ALL.Oncogene · 2024Article
- NOTCH3 as a prognostic biomarker and its correlation with immune infiltration in gastrointestinal cancers.Scientific reports · 2024Article
- Pin1-catalyzed conformational regulation after phosphorylation: A distinct checkpoint in cell signaling and drug discovery.Science signaling · 2024Review
- Review
- Nanocarrier of Pin1 inhibitor based on supercritical fluid technology inhibits cancer metastasis by blocking multiple signaling pathways.Regenerative biomaterials · 2023Article
- Hydroxylation of the NOTCH1 intracellular domain regulates Notch signaling dynamics.Cell death & disease · 2022Article
- Opsonin-Deficient Nucleoproteic Corona Endows UnPEGylated Liposomes with Stealth PropertiesACS nano · 2022Article
- Notch-Signaling Deregulation Induces Myeloid-Derived Suppressor Cells in T-Cell Acute Lymphoblastic Leukemia.Frontiers in immunology · 2022Article
- Targeting Notch to Maximize Chemotherapeutic Benefits: Rationale, Advanced Strategies, and Future Perspectives.Cancers · 2021Review
- Roles of peptidyl-prolyl isomerase Pin1 in disease pathogenesis.Theranostics · 2021Review
- ProAlanase is an Effective Alternative to Trypsin for Proteomics Applications and Disulfide Bond Mapping.Molecular & cellular proteomics : MCP · 2020Article
- Notch3 contributes to T-cell leukemia growth via regulation of the unfolded protein response.Oncogenesis · 2020Article
- Current Trends in ATRA Delivery for Cancer Therapy.Pharmaceutics · 2020Review
- Notch3 in Development, Health and Disease.Biomolecules · 2020Review
- Targeting PIN-1 Attenuates GCB DLBCL Cell Proliferation Through Inhibition of PI3K/AKT Signaling.OncoTargets and therapy · 2020Article
- Function of PIN1 in Cancer Development and Its Inhibitors as Cancer Therapeutics.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deregulated Notch signaling is associated with T-cell Acute Lymphoblastic Leukemia (T-ALL) development and progression. Increasing evidence reveals that Notch pathway has an important role in the invasion ability of tumor cells, including leukemia, although the underlying molecular mechanisms remain mostly unclear. Here, we show that Notch3 is a novel target protein of the prolyl-isomerase Pin1, which is able to regulate Notch3 protein processing and to stabilize the cleaved product, leading to the increased expression of the intracellular domain (N3IC), finally enhancing Notch3-dependent invasiveness properties. We demonstrate that the combined inhibition of Notch3 and Pin1 in the Notch3-overexpressing human leukemic TALL-1 cells reduces their high invasive potential, by decreasing the expression of the matrix metalloprotease MMP9. Consistently, Pin1 depletion in a mouse model of Notch3-induced T-ALL, by reducing N3IC expression and signaling, impairs the expansion/invasiveness of CD4(+)CD8(+) DP cells in peripheral lymphoid and non-lymphoid organs. Notably, in in silico gene expression analysis of human T-ALL samples we observed a significant correlation between Pin1 and Notch3 expression levels, which may further suggest a key role of the newly identified Notch3-Pin1 axis in T-ALL aggressiveness and progression. Thus, combined suppression of Pin1 and Notch3 proteins may be exploited as an additional target therapy for T-ALL.
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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.