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Cytoplasmic cyclin D1 regulates cell invasion and metastasis through the phosphorylation of paxillin

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  • Noel P. Fusté

    (Cell Cycle Lab, Institut de Recerca Biomèdica de Lleida (IRBLleida), and Departament de Ciències Mèdiques Bàsiques; Facultat de Medicina; Universitat de Lleida
    Facultat de Medicina)

  • Rita Fernández-Hernández

    (Cell Cycle Lab, Institut de Recerca Biomèdica de Lleida (IRBLleida), and Departament de Ciències Mèdiques Bàsiques; Facultat de Medicina; Universitat de Lleida
    Facultat de Medicina
    Present address: Cell Cycle Group, Cancer Epigenetics and Biology Program (PEBC), Institut d’Investigació Biomèdica de Bellvitge (IDIBELL), Barcelona, Catalonia, Spain.)

  • Tània Cemeli

    (Cell Cycle Lab, Institut de Recerca Biomèdica de Lleida (IRBLleida), and Departament de Ciències Mèdiques Bàsiques; Facultat de Medicina; Universitat de Lleida
    Facultat de Medicina)

  • Cristina Mirantes

    (Oncopathology Lab, Institut de Recerca Biomèdica de Lleida (IRBLleida), and Departament de Ciències Mèdiques Bàsiques; Facultat de Medicina; Universitat de Lleida
    Facultat de Medicina)

  • Neus Pedraza

    (Cell Cycle Lab, Institut de Recerca Biomèdica de Lleida (IRBLleida), and Departament de Ciències Mèdiques Bàsiques; Facultat de Medicina; Universitat de Lleida
    Facultat de Medicina)

  • Marta Rafel

    (Cell Cycle Lab, Institut de Recerca Biomèdica de Lleida (IRBLleida), and Departament de Ciències Mèdiques Bàsiques; Facultat de Medicina; Universitat de Lleida
    Facultat de Medicina)

  • Jordi Torres-Rosell

    (Cell Cycle Lab, Institut de Recerca Biomèdica de Lleida (IRBLleida), and Departament de Ciències Mèdiques Bàsiques; Facultat de Medicina; Universitat de Lleida
    Facultat de Medicina)

  • Neus Colomina

    (Cell Cycle Lab, Institut de Recerca Biomèdica de Lleida (IRBLleida), and Departament de Ciències Mèdiques Bàsiques; Facultat de Medicina; Universitat de Lleida
    Facultat de Medicina)

  • Francisco Ferrezuelo

    (Cell Cycle Lab, Institut de Recerca Biomèdica de Lleida (IRBLleida), and Departament de Ciències Mèdiques Bàsiques; Facultat de Medicina; Universitat de Lleida
    Facultat de Medicina)

  • Xavier Dolcet

    (Oncopathology Lab, Institut de Recerca Biomèdica de Lleida (IRBLleida), and Departament de Ciències Mèdiques Bàsiques; Facultat de Medicina; Universitat de Lleida
    Facultat de Medicina)

  • Eloi Garí

    (Cell Cycle Lab, Institut de Recerca Biomèdica de Lleida (IRBLleida), and Departament de Ciències Mèdiques Bàsiques; Facultat de Medicina; Universitat de Lleida
    Facultat de Medicina)

Abstract

Cyclin D1 (Ccnd1) together with its binding partner Cdk4 act as a transcriptional regulator to control cell proliferation and migration, and abnormal Ccnd1·Cdk4 expression promotes tumour growth and metastasis. While different nuclear Ccnd1·Cdk4 targets participating in cell proliferation and tissue development have been identified, little is known about how Ccnd1·Cdk4 controls cell adherence and invasion. Here, we show that the focal adhesion component paxillin is a cytoplasmic substrate of Ccnd1·Cdk4. This complex phosphorylates a fraction of paxillin specifically associated to the cell membrane, and promotes Rac1 activation, thereby triggering membrane ruffling and cell invasion in both normal fibroblasts and tumour cells. Our results demonstrate that localization of Ccnd1·Cdk4 to the cytoplasm does not simply act to restrain cell proliferation, but constitutes a functionally relevant mechanism operating under normal and pathological conditions to control cell adhesion, migration and metastasis through activation of a Ccnd1·Cdk4-paxillin-Rac1 axis.

Suggested Citation

  • Noel P. Fusté & Rita Fernández-Hernández & Tània Cemeli & Cristina Mirantes & Neus Pedraza & Marta Rafel & Jordi Torres-Rosell & Neus Colomina & Francisco Ferrezuelo & Xavier Dolcet & Eloi Garí, 2016. "Cytoplasmic cyclin D1 regulates cell invasion and metastasis through the phosphorylation of paxillin," Nature Communications, Nature, vol. 7(1), pages 1-14, September.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11581
    DOI: 10.1038/ncomms11581
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