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Requirement for YAP1 signaling in myxoid liposarcoma

Marcel Trautmann1,2, Ya-Yun Cheng3,4, Patrizia Jensen3,4

  • 1Gerhard-Domagk-Institute of Pathology, Münster University Hospital, Münster, Germany.

EMBO Molecular Medicine
|March 23, 2019
PubMed

Insights

Myxoid liposarcomas (MLS) rely on YAP1, a key protein in cell growth. Inhibiting YAP1 effectively stops MLS tumor growth, offering a new therapeutic target for this cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Myxoid liposarcomas (MLS) are malignant tumors originating from fat cells.
  • The FUS-DDIT3 fusion gene drives MLS, but its exact role in cancer development is unclear.
  • Targeting MLS cells specifically remains a challenge.

Purpose of the Study:

  • To investigate the mechanisms driving sarcomagenesis in MLS.
  • To identify potential therapeutic targets for MLS treatment.
  • To explore the role of YAP1 in MLS development.

Main Methods:

  • Functional genomic screening in FUS-DDIT3-expressing cells.
  • Analysis of YAP1 expression, localization, and activity in MLS.
  • Pharmacological inhibition of YAP1 in vitro and in vivo models.

Main Results:

  • FUS-DDIT3-driven cells and MLS lines are dependent on YAP1.
  • Increased YAP1 activity is a characteristic of human MLS.
  • FUS-DDIT3 enhances YAP1 expression, nuclear import, and activity, with physical interaction in the nucleus.
  • YAP1 inhibition reduces MLS cell proliferation in vitro and tumor growth in vivo.

Conclusions:

  • Overactive YAP1 signaling is a central feature of MLS development.
  • YAP1 represents a promising novel therapeutic target for myxoid liposarcomas.
Keywords:
FUS‐DDIT3Hippo pathwayYAP1myxoid liposarcomaverteporfin

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