IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v10y2019i1d10.1038_s41467-019-09755-0.html
   My bibliography  Save this article

YAP-independent mechanotransduction drives breast cancer progression

Author

Listed:
  • Joanna Y. Lee

    (Stanford University)

  • Jessica K. Chang

    (Department of Genetics, Stanford University School of Medicine)

  • Antonia A. Dominguez

    (Stanford University
    Stanford University
    Stanford University)

  • Hong-pyo Lee

    (Stanford University)

  • Sungmin Nam

    (Stanford University)

  • Julie Chang

    (Stanford University)

  • Sushama Varma

    (Stanford University School of Medicine)

  • Lei S. Qi

    (Stanford University
    Stanford University)

  • Robert B. West

    (Stanford University School of Medicine)

  • Ovijit Chaudhuri

    (Stanford University)

Abstract

Increased tissue stiffness is a driver of breast cancer progression. The transcriptional regulator YAP is considered a universal mechanotransducer, based largely on 2D culture studies. However, the role of YAP during in vivo breast cancer remains unclear. Here, we find that mechanotransduction occurs independently of YAP in breast cancer patient samples and mechanically tunable 3D cultures. Mechanistically, the lack of YAP activity in 3D culture and in vivo is associated with the absence of stress fibers and an order of magnitude decrease in nuclear cross-sectional area relative to 2D culture. This work highlights the context-dependent role of YAP in mechanotransduction, and establishes that YAP does not mediate mechanotransduction in breast cancer.

Suggested Citation

  • Joanna Y. Lee & Jessica K. Chang & Antonia A. Dominguez & Hong-pyo Lee & Sungmin Nam & Julie Chang & Sushama Varma & Lei S. Qi & Robert B. West & Ovijit Chaudhuri, 2019. "YAP-independent mechanotransduction drives breast cancer progression," Nature Communications, Nature, vol. 10(1), pages 1-9, December.
  • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-09755-0
    DOI: 10.1038/s41467-019-09755-0
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/s41467-019-09755-0
    File Function: Abstract
    Download Restriction: no

    File URL: https://libkey.io/10.1038/s41467-019-09755-0?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-09755-0. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.