ArticleMolecular and cellular biology2008
Degradation of the tumor suppressor PML by Pin1 contributes to the cancer phenotype of breast cancer MDA-MB-231 cells.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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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.
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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
58 citing papers in PubMed, 92 citations in OpenAlex.
- Proline-directed phosphorylation and prolyl isomerization oppose each other to regulate PSD-95 ubiquitination and excitatory synaptic plasticity.Frontiers in molecular neuroscience · 2026Article
- Pin1-catalyzed conformational regulation after phosphorylation: A distinct checkpoint in cell signaling and drug discovery.Science signaling · 2024Review
- Review
- Reciprocal antagonism of PIN1-APC/CNature communications · 2024Article
- Review
- Targeting peptidyl-prolyl isomerase 1 in experimental pulmonary arterial hypertension.The European respiratory journal · 2022Article
- A Pin1/PML/P53 axis activated by retinoic acid inHaematologica · 2021Article
- Targeting Pin1 for Modulation of Cell Motility and Cancer Therapy.Biomedicines · 2021Review
- Review
- Roles of peptidyl-prolyl isomerase Pin1 in disease pathogenesis.Theranostics · 2021Review
- Protein sumoylation with SUMO1 promoted by Pin1 in glioma stem cells augments glioblastoma malignancy.Neuro-oncology · 2020Article
- The HECT E3 Ligase E6AP/UBE3A as a Therapeutic Target in Cancer and Neurological Disorders.Cancers · 2020Review
- Vulnerabilities in mIDH2 AML confer sensitivity to APL-like targeted combination therapy.Cell research · 2019Article
- Synthetic lethality of cytolytic HSV-1 in cancer cells with ATRX and PML deficiency.Journal of cell science · 2019Article
- PML: Regulation and multifaceted function beyond tumor suppression.Cell & bioscience · 2018Review
- Gears-In-Motion: The Interplay of WW and PPIase Domains in Pin1.Frontiers in oncology · 2018Review
- Arsenic trioxide and angiotensin II have inhibitory effects on HERG protein expression: Evidence for the role of PML SUMOylation.Oncotarget · 2017Article
- Generation of a cell-permeable cycloheptapeptidyl inhibitor against the peptidyl-prolyl isomerase Pin1.Organic & biomolecular chemistry · 2017Article
- Manipulating PML SUMOylation via Silencing UBC9 and RNF4 Regulates Cardiac Fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2017Article
- Neighboring phosphoSer-Pro motifs in the undefined domain of IRAK1 impart bivalent advantage for Pin1 binding.The FEBS journal · 2016Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Promyelocytic leukemia protein (PML) is an important regulator due to its role in numerous cellular processes including apoptosis, viral infection, senescence, DNA damage repair, and cell cycle regulation. Despite the role of PML in many cellular functions, little is known about the regulation of PML itself. We show that PML stability is regulated through interaction with the peptidyl-prolyl cis-trans isomerase Pin1. This interaction is mediated through four serine-proline motifs in the C terminus of PML. Binding to Pin1 results in degradation of PML in a phosphorylation-dependent manner. Furthermore, our data indicate that sumoylation of PML blocks the interaction, thus preventing degradation of PML by this pathway. Functionally, we show that in the MDA-MB-231 breast cancer cell line modulating levels of Pin1 affects steady-state levels of PML. Furthermore, degradation of PML due to Pin1 acts both to protect these cells from hydrogen peroxide-induced death and to increase the rate of proliferation. Taken together, our work defines a novel mechanism by which sumoylation of PML prevents Pin1-dependent degradation. This interaction likely occurs in numerous cell lines and may be a pathway for oncogenic transformation.
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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.