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The spectraplakin Dystonin antagonizes YAP activity and suppresses tumourigenesis

Praachi B Jain1,2,3, Patrícia S Guerreiro1,2,3, Sara Canato1,2,3

  • 1Instituto Gulbenkian de Ciência, Rua da Quinta Grande 6, P-2780-156, Oeiras, Portugal.

Scientific Reports
|December 29, 2019
PubMed

Insights

Dystonin (DST) acts as a tumor suppressor in breast cancer by restraining cell growth and promoting adhesion. Loss of Dystonin correlates with cancer progression and may serve as a prognostic biomarker.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Biology

Background:

  • Aberrant Dystonin (DST) expression is linked to various cancers, including breast cancer.
  • The specific role of Dystonin in cancer development remains largely uncharacterized.

Purpose of the Study:

  • To investigate Dystonin's function in breast cancer and elucidate its molecular mechanism.
  • To identify Dystonin as a potential tumor suppressor in breast epithelial cells.

Main Methods:

  • Utilized MCF10A cells to assess Dystonin's impact on cell growth, self-renewal, and drug resistance.
  • Examined Dystonin's effects on focal adhesion, cell spreading, and signaling pathways (YAP/LATS).
  • Investigated Dystonin's role in vivo using Drosophila models and analyzed Dystonin isoform expression in human breast tumor samples.

Main Results:

  • Dystonin depletion in MCF10A cells led to increased cell growth, anchorage-independent growth, and doxorubicin resistance.
  • Dystonin maintains focal adhesion integrity, promotes cell spreading, and inhibits YAP activation.
  • Loss of Dystonin isoforms (BPAG1eA and BPAG1e) was observed in breast tumors and correlated with oncogene activation, suggesting a tumor suppressor role.

Conclusions:

  • Dystonin functions as a tumor suppressor in breast cancer by regulating cell growth and adhesion pathways.
  • Downregulation of Dystonin isoforms BPAG1eA and BPAG1e contributes to malignant transformation.
  • Dystonin loss represents a potential prognostic biomarker for breast cancer.

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