IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v9y2018i1d10.1038_s41467-018-07127-8.html
   My bibliography  Save this article

TAp73-induced phosphofructokinase-1 transcription promotes the Warburg effect and enhances cell proliferation

Author

Listed:
  • Le Li

    (Tsinghua University; Collaborative Innovation Center for Cancer Medicine)

  • Lijia Li

    (Tsinghua University; Collaborative Innovation Center for Cancer Medicine)

  • Wei Li

    (State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College)

  • Taiqi Chen

    (Tsinghua University; Collaborative Innovation Center for Cancer Medicine)

  • Bin Zou

    (Tsinghua University; Collaborative Innovation Center for Cancer Medicine)

  • Lina Zhao

    (Tsinghua University; Collaborative Innovation Center for Cancer Medicine)

  • Huili Wang

    (Tsinghua University)

  • Xueying Wang

    (Tsinghua University; Collaborative Innovation Center for Cancer Medicine)

  • Lina Xu

    (Tsinghua University; Collaborative Innovation Center for Cancer Medicine)

  • Xiaohui Liu

    (Tsinghua University; Collaborative Innovation Center for Cancer Medicine)

  • Dong Wang

    (Tsinghua University)

  • Bo Li

    (Sun Yat-sen University)

  • Tak W. Mak

    (The Campbell Family Institute for Breast Cancer Research, Princess Margaret Hospital)

  • Wenjing Du

    (State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College)

  • Xiaolu Yang

    (University of Pennsylvania)

  • Peng Jiang

    (Tsinghua University; Collaborative Innovation Center for Cancer Medicine)

Abstract

The Warburg effect is a prominent metabolic feature associated with neoplastic diseases; however, the underlying mechanism remains incompletely understood. TAp73, a structural homolog of the tumor suppressor p53, is frequently overexpressed in human tumors, indicating a proliferative advantage that it can confer to tumor cells. Here we show that TAp73 stimulates the expression of phosphofructokinase-1, liver type (PFKL), which catalyzes the committed step in glycolysis. Through this regulation, TAp73 enhances glucose consumption and lactate excretion, promoting the Warburg effect. By activating PFKL, TAp73 also increases ATP production and bolsters anti-oxidant defense. TAp73 deficiency results in a pronounced reduction in tumorigenic potential, which can be rescued by forced PFKL expression. These findings establish TAp73 as a critical regulator of glycolysis and reveal a mechanism by which tumor cells achieve the Warburg effect to enable oncogenic growth.

Suggested Citation

  • Le Li & Lijia Li & Wei Li & Taiqi Chen & Bin Zou & Lina Zhao & Huili Wang & Xueying Wang & Lina Xu & Xiaohui Liu & Dong Wang & Bo Li & Tak W. Mak & Wenjing Du & Xiaolu Yang & Peng Jiang, 2018. "TAp73-induced phosphofructokinase-1 transcription promotes the Warburg effect and enhances cell proliferation," Nature Communications, Nature, vol. 9(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-07127-8
    DOI: 10.1038/s41467-018-07127-8
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/s41467-018-07127-8
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/s41467-018-07127-8?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
    ---><---

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Cao Wang & Shupei Qiao & Yufang Zhao & Hui Tian & Wei Yan & Xiaolu Hou & Ruiqi Wang & Bosong Zhang & Chaofan Yang & Fuxing Zhu & Yanwen Jiao & Jiaming Jin & Yue Chen & Weiming Tian, 2023. "The KLF7/PFKL/ACADL axis modulates cardiac metabolic remodelling during cardiac hypertrophy in male mice," Nature Communications, Nature, vol. 14(1), pages 1-18, December.

    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:9:y:2018:i:1:d:10.1038_s41467-018-07127-8. 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.