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Updated: May 13, 2025

Induction and Analysis of Epithelial to Mesenchymal Transition
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Epithelial cell-fate switch triggering ectopic ligand-receptor-mediated JAK-STAT signaling promotes tumorigenesis in

Jiaqi Li1, Kiichiro Taniguchi1, Weiran Ye1

  • 1Laboratory of Genetics, Graduate School of Biostudies, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 607-8501, Japan.

Iscience
|April 15, 2025
PubMed

Insights

Epithelial deformation, triggered by cell-fate changes, promotes Ras-activated tumor growth in Drosophila. This involves mislocalization of the Domeless receptor, activating JAK-STAT signaling and driving cancer progression.

Area of Science:

  • Developmental Biology
  • Cancer Biology
  • Genetics

Background:

  • Epithelial architecture disruption is a key feature of cancers.
  • The role of epithelial deformation in tumor progression remains unclear.

Purpose of the Study:

  • To investigate how epithelial deformation influences Ras-activated tumor growth.
  • To identify genetic factors and mechanisms linking cell-fate changes to cancer progression.

Main Methods:

  • Genetic screen in Drosophila eye disc to identify mutations affecting Ras-activated tumor growth.
  • Mis-expression of Abd-B to induce cell-fate switch and observe effects on tumor growth.
  • Analysis of receptor mislocalization and signaling pathway activation.

Main Results:

  • The eyes absent (eya) gene mutation compromised growth but synergized with RasV12 for massive overgrowth.
  • Mis-expression of Abd-B induced cell-fate switch and massive RasV12 overgrowth.
  • Cell-fate switch caused epithelial invagination and Domeless receptor mislocalization, leading to JAK-STAT activation that cooperated with RasV12.

Conclusions:

  • Cell-fate switch and subsequent epithelial deformation create a cancer-prone environment.
  • Epithelial deformation, receptor mislocalization, and JAK-STAT signaling cooperate with RasV12 to drive tumor progression.
Keywords:
CancerCell biologyOrganizational aspects of cell biology

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