ArticleMolecular and cellular biology2006
Pin1 regulates centrosome duplication, and its overexpression induces centrosome amplification, chromosome instability, and oncogenesis.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 119 citations in OpenAlex.
- Pre-clinical evaluation of a potent and effective Pin1-degrading agent in pancreatic cancer.Molecular therapy. Oncology · 2025Article
- PIN1 Prolyl Isomerase Promotes Initiation and Progression of Bladder Cancer through the SREBP2-Mediated Cholesterol Biosynthesis Pathway.Cancer discovery · 2025Article
- Pin1-catalyzed conformational regulation after phosphorylation: A distinct checkpoint in cell signaling and drug discovery.Science signaling · 2024Review
- The mechanisms of Pin1 as targets for cancer therapy.Frontiers in immunology · 2024Review
- Review
- Non-POU Domain-Containing Octomer-Binding (NONO) protein expression and stability promotes the tumorigenicity and activation of Akt/MAPK/β-catenin pathways in human breast cancer cells.Cell communication and signaling : CCS · 2023Article
- Targeting Pin1 for Modulation of Cell Motility and Cancer Therapy.Biomedicines · 2021Review
- Centrosome amplification: a quantifiable cancer cell trait with prognostic value in solid malignancies.Cancer metastasis reviews · 2021Review
- Peptidyl-ProlylFrontiers in cell and developmental biology · 2020Review
- Post-translational Modifications of the Peptidyl-Prolyl Isomerase Pin1.Frontiers in cell and developmental biology · 2020Review
- Function of PIN1 in Cancer Development and Its Inhibitors as Cancer Therapeutics.Frontiers in cell and developmental biology · 2020Review
- Subcellular localization of mutated β-catenins with different incidences ofFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Identification of Prolyl isomerase Pin1 as a novel positive regulator of YAP/TAZ in breast cancer cells.Scientific reports · 2019Article
- Oncogenic Hijacking of the PIN1 Signaling Network.Frontiers in oncology · 2019Review
- Death-Associated Protein Kinase 1 as a Promising Drug Target in Cancer and Alzheimer's Disease.Recent patents on anti-cancer drug discovery · 2019Review
- Cytoplasmic Pin1 expression is increased in human cutaneous melanoma and predicts poor prognosis.Scientific reports · 2018Article
- Prolyl isomerase Pin1: a promoter of cancer and a target for therapy.Cell death & disease · 2018Review
- Arsenic targets Pin1 and cooperates with retinoic acid to inhibit cancer-driving pathways and tumor-initiating cells.Nature communications · 2018Article
- PIN1 in Cell Cycle Control and Cancer.Frontiers in pharmacology · 2018Review
- Centrosome aberrations and chromosome instability contribute to tumorigenesis and intra-tumor heterogeneity.Journal of cancer metastasis and treatment · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Phosphorylation on Ser/Thr-Pro motifs is a major mechanism regulating many events involved in cell proliferation and transformation, including centrosome duplication, whose defects have been implicated in oncogenesis. Certain phosphorylated Ser/Thr-Pro motifs can exist in two distinct conformations whose conversion in certain proteins is catalyzed specifically by the prolyl isomerase Pin1. Pin1 is prevalently overexpressed in human cancers and is important for the activation of multiple oncogenic pathways, and its deletion suppresses the ability of certain oncogenes to induce cancer in mice. However, little is known about the role of Pin1 in centrosome duplication and the significance of Pin1 overexpression in cancer development in vivo. Here we show that Pin1 overexpression correlates with centrosome amplification in human breast cancer tissues. Furthermore, Pin1 localizes to and copurifies with centrosomes in interphase but not mitotic cells. Moreover, Pin1 ablation in mouse embryonic fibroblasts drastically delays centrosome duplication without affecting DNA synthesis and Pin1 inhibition also suppresses centrosome amplification in S-arrested CHO cells. In contrast, overexpression of Pin1 drives centrosome duplication and accumulation, resulting in chromosome missegregation, aneuploidy, and transformation in nontransformed NIH 3T3 cells. More importantly, transgenic overexpression of Pin1 in mouse mammary glands also potently induces centrosome amplification, eventually leading to mammary hyperplasia and malignant mammary tumors with overamplified centrosomes. These results demonstrate for the first time that the phosphorylation-specific isomerase Pin1 regulates centrosome duplication and its deregulation can induce centrosome amplification, chromosome instability, and oncogenesis.
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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.