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    The Prolyl Isomerase Pin1 Acts Synergistically with CDK2 to Regulate the Basal Activity of Estrogen Receptor α in Breast Cancer

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    Name:
    The prolyl isomerase Pin1 acts ...
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    Genre
    Journal Article
    Date
    2013-02-04
    Author
    Lucchetti, C
    Caligiuri, I
    Toffoli, G
    Giordano, A
    Rizzolio, F
    Subject
    Binding Sites
    Breast Neoplasms
    Cell Line, Tumor
    Cyclin-Dependent Kinase 2
    Drug Resistance, Neoplasm
    Estrogen Receptor alpha
    Female
    Gene Expression Regulation, Neoplastic
    Humans
    Mutagenesis, Site-Directed
    NIMA-Interacting Peptidylprolyl Isomerase
    Peptidylprolyl Isomerase
    Phosphatidylinositol 3-Kinases
    Phosphorylation
    Protein Binding
    Serine
    Signal Transduction
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    Permanent link to this record
    http://hdl.handle.net/20.500.12613/5414
    
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    DOI
    10.1371/journal.pone.0055355
    Abstract
    In hormone receptor-positive breast cancers, most tumors in the early stages of development depend on the activity of the estrogen receptor and its ligand, estradiol. Anti-estrogens, such as tamoxifen, have been used as the first line of therapy for over three decades due to the fact that they elicit cell cycle arrest. Unfortunately, after an initial period, most cells become resistant to hormonal therapy. Peptidylprolyl isomerase 1 (Pin1), a protein overexpressed in many tumor types including breast, has been demonstrated to modulate ERalpha activity and is involved in resistance to hormonal therapy. Here we show a new mechanism through which CDK2 drives an ERalpha-Pin1 interaction under hormone- and growth factor-free conditions. The PI3K/AKT pathway is necessary to activate CDK2, which phosphorylates ERalphaSer294, and mediates the binding between Pin1 and ERalpha. Site-directed mutagenesis demonstrated that ERalphaSer294 is essential for Pin1-ERalpha interaction and modulates ERalpha phosphorylation on Ser118 and Ser167, dimerization and activity. These results open up new drug treatment opportunities for breast cancer patients who are resistant to anti-estrogen therapy. © 2013 Lucchetti et al.
    Citation to related work
    Public Library of Science (PLoS)
    Has part
    PLoS ONE
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    ae974a485f413a2113503eed53cd6c53
    http://dx.doi.org/10.34944/dspace/5396
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