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TEADs mediate nuclear retention of TAZ to promote oncogenic transformation

Siew Wee Chan1, Chun Jye Lim, Li Shen Loo

  • 1Cancer and Developmental Cell Biology Division, Institute of Molecular and Cell Biology, Singapore 138673, Singapore.

The Journal of Biological Chemistry
|March 28, 2009
PubMed

Insights

The transcriptional coactivators YAP and TAZ are key in breast cancer. This study reveals that TEAD factors mediate TAZ

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • The Hippo pathway regulates YAP and TAZ, crucial transcriptional coactivators.
  • Elevated TAZ expression is linked to invasive breast cancer, promoting migration and invasion.
  • The precise mechanism of TAZ's oncogenic activity remains undefined.

Purpose of the Study:

  • To elucidate the mechanism by which TAZ contributes to breast cancer progression.
  • To investigate the interaction between TAZ and TEAD transcriptional factors.
  • To determine the role of TEAD interaction in TAZ's nuclear localization and oncogenic function.

Main Methods:

  • Investigated TAZ-TEAD interactions using biochemical assays.
  • Utilized knockdown of TEADs to assess TAZ-mediated oncogenic transformation in MCF10A cells.
  • Employed site-directed mutagenesis (S89A) to uncouple TAZ from Hippo regulation.
  • Performed live cell imaging of TAZ and its mutants to track nuclear localization.

Main Results:

  • TAZ directly interacts with TEAD transcriptional factors.
  • Knockdown of TEADs abrogates TAZ-induced oncogenic transformation of MCF10A cells.
  • Specific N-terminal residues of TAZ are critical for both TEAD interaction and cellular transformation.
  • TAZ mutants unable to interact with TEADs exhibit impaired nuclear accumulation.
  • TEAD interaction is essential for TAZ's nuclear retention.

Conclusions:

  • TEADs are essential interaction partners for TAZ in mediating oncogenic transformation.
  • TEAD interaction regulates TAZ's nuclear retention, a key step in its transforming ability.
  • This study uncovers a novel mechanism involving TEADs in controlling TAZ function in breast cancer.

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