Yorkie and JNK Control Tumorigenesis in Drosophila Cells with Cytokinesis Failure

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Stephan U Gerlach1, Teresa Eichenlaub1, Héctor Herranz1

  • 1Department of Cellular and Molecular Medicine, University of Copenhagen, Blegdamsvej 3, Copenhagen 2200 N, Denmark.

Cell Reports
|May 3, 2018
PubMed

Insights

Cytokinesis failure can lead to polyploidy and cancer. In Drosophila, JNK pathway activation induces cell death, but Yorkie protein can bypass this barrier, promoting tumor formation.

Area of Science:

  • Cell Biology
  • Cancer Biology
  • Developmental Biology

Background:

  • Cytokinesis failure can lead to polyploidy, aneuploidy, and tumor formation.
  • Tumor suppressor mechanisms exist but their universal applicability is debated.
  • Investigating cytokinesis failure consequences in vivo is crucial.

Purpose of the Study:

  • To investigate the consequences of cytokinesis failure in Drosophila epithelial cells in vivo.
  • To elucidate the mechanisms by which cells bypass tumor suppression after cytokinesis failure.

Main Methods:

  • Utilized Drosophila epithelial cells for in vivo studies.
  • Analyzed the JNK pathway activation in response to cytokinesis defects.
  • Investigated the role of Yorkie and Cdc25/string in tumorigenesis.

Main Results:

  • Cytokinesis defects activate the JNK pathway, downregulating DIAP1 and inducing apoptosis.
  • The Yorkie protein overcomes JNK-mediated tumor suppression.
  • Yorkie regulates Cdc25/string, driving tumorigenesis in the context of cytokinesis failure.

Conclusions:

  • The JNK pathway plays a significant role in epithelial cells with defective cytokinesis.
  • Yorkie provides a mechanism for emerging tumor cells to bypass tumor-suppressive barriers.
  • Understanding these pathways is key to developing cancer therapies.
Keywords:
CDC25DrosophilaHippo pathwayJNKcancercell cyclecytokinesis failuregenomic instability

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