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SOX2 antagonizes WWC1 to drive YAP1 activation in esophageal squamous cell carcinoma

Yuhang Chai1, Qihang Li1, Hongying Zhao2

  • 1Department of Pathology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases/the First Affiliated Hospital, Shihezi University School of Medicine, Shihezi, China.

Cancer Medicine
|September 28, 2019
PubMed

Insights

SOX2, ACTL6A, and TP63 are amplified in esophageal squamous cell carcinoma (ESCC). These factors repress WWC1, activating the Hippo-YAP1 pathway, driving tumor progression and chemoresistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • The role of SOX2, ACTL6A, and TP63 in the Hippo-YAP1 pathway in esophageal squamous cell carcinoma (ESCC) is not well understood.
  • Investigating these interactions is crucial for understanding ESCC pathogenesis.

Purpose of the Study:

  • To elucidate the interaction between SOX2, ACTL6A, TP63, and the Hippo-YAP1 pathway in ESCC.
  • To determine the functional consequences of this interaction on tumor progression and chemoresistance.

Main Methods:

  • Analysis of gene amplification and expression in ESCC samples.
  • Chromatin immunoprecipitation sequencing to identify SOX2 binding sites.
  • Correlation analysis between gene expression and YAP1 localization.
  • Gain-of-function and knockdown experiments in ESCC cell lines.

Main Results:

  • SOX2, ACTL6A, and TP63 are co-amplified and upregulated in ESCC.
  • SOX2 directly represses WWC1, a Hippo-YAP1 pathway regulator.
  • SOX2 promotes nuclear YAP1 expression, enhancing cell migration, invasion, and cisplatin chemoresistance.
  • WWC1 ectopic expression or SOX2 knockdown suppresses SOX2-induced phenotypes.

Conclusions:

  • A novel SOX2-WWC1-YAP1 axis is identified in ESCC.
  • This axis drives tumor progression and chemoresistance.
  • Targeting this axis presents a potential therapeutic strategy for SOX2-dependent ESCC.
Keywords:
ESCCSOX2WWC1YAP1

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