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Blocking YAP1-Liprin-β2 interaction impedes metastasis and promotes tumor suppression in head and neck squamous

Seon Rang Woo1, Joo Kyung Noh2, Min Kyeong Lee2

  • 1Department of Otolaryngology-Head and Neck Surgery, Kyung Hee University Medical Center, College of Medicine Kyung Hee University, #1 Hoegi-dong, Dongdaemun-gu, Seoul, 02447, Republic of Korea.

Scientific Reports
|July 24, 2025
PubMed

Insights

The YAP1-PPFIBP2 axis drives tumor aggressiveness in head and neck squamous cell carcinoma (HNSCC) by promoting epithelial-mesenchymal transition (EMT), invasion, and migration. Targeting this axis offers a potential therapeutic strategy for HNSCC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Head and neck squamous cell carcinoma (HNSCC) is characterized by aggressive tumor behavior, including invasion and metastasis.
  • The epithelial-mesenchymal transition (EMT) is a key process driving cancer cell motility and invasiveness.
  • Understanding the molecular regulators of EMT in HNSCC is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of the YAP1-PPFIBP2 axis in regulating EMT, invasion, and migration in HNSCC.
  • To determine if targeting this axis can inhibit HNSCC progression.
  • To explore the prognostic significance of the YAP1-PPFIBP2 pathway in HNSCC.

Main Methods:

  • In vitro cell culture assays (siRNA knockdown, overexpression) in HNSCC cell lines (SNU1041, SCC9, SCC25).
  • Genomic analyses to assess YAP1 and PPFIBP2 expression.
  • Pharmacological inhibition of YAP1 using CA3.
  • Assessment of EMT markers, invasion, and migration.

Main Results:

  • YAP1 upregulation of EMT was confirmed by suppression of PPFIBP2/liprin-β2 expression.
  • YAP1 knockdown reduced HNSCC cell invasion and migration, effects reversed by siPPFIBP2.
  • YAP1 overexpression enhanced EMT markers and invasive behavior.
  • Pharmacological inhibition of YAP1 decreased EMT markers, invasion, and migration.
  • The YAP1-PPFIBP2 axis activity correlated with poorer prognostic outcomes in HNSCC.

Conclusions:

  • The YAP1-PPFIBP2 axis is a critical mediator of tumor aggressiveness and metastatic potential in HNSCC.
  • Targeting the YAP1-PPFIBP2 pathway represents a promising therapeutic strategy for HNSCC treatment.
  • This study provides novel insights into the molecular mechanisms underlying HNSCC progression.

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