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Updated: May 6, 2026

A Protocol for Genetic Induction and Visualization of Benign and Invasive Tumors in Cephalic Complexes of Drosophila melanogaster
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A Protocol for Genetic Induction and Visualization of Benign and Invasive Tumors in Cephalic Complexes of Drosophila melanogaster

Published on: September 11, 2013

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Src42A modulates tumor invasion and cell death via Ben/dUev1a-mediated JNK activation in Drosophila

X Ma1, Y Shao, H Zheng

  • 1Department of Interventional Radiology, Shanghai Key Laboratory of Signaling and Disease Research, Shanghai 10th People's Hospital, School of Life Science and Technology, Tongji University, Shanghai 200092, China.

Cell Death & Disease
|October 19, 2013
PubMed

Insights

Loss of cell polarity genes and oncogenic Ras cooperate to drive tumor invasion, modulated by Src42A and the JNK pathway. The Bendless/dUev1a complex is crucial for this Src42A-induced migration and invasion.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Oncology

Background:

  • Cell polarity loss cooperates with oncogenic Ras to drive tumor growth and invasion.
  • The c-Jun N-terminal Kinase (JNK) signaling pathway is critical for Ras-driven tumor invasion.

Purpose of the Study:

  • Identify key modulators of Ras/polarity loss-driven tumor invasion and cell migration.
  • Investigate the role of the Bendless (Ben)/dUev1a ubiquitin E2 complex in Src42A-induced, JNK-mediated cell migration.
  • Explore the oncogenic potential of Ben/dUev1a and its mammalian homologs.

Main Methods:

  • Genetic screening in Drosophila to identify novel regulators.
  • Analysis of gene interactions in tumor growth and invasion models.
  • Assessment of cell migration, MMP1 production, and cell death.

Main Results:

  • Src42A identified as a key modulator of tumor invasion and cell migration.
  • The Ben/dUev1a complex is essential for Src42A-induced, JNK-mediated cell migration.
  • Ectopic Ben/dUev1a expression promotes invasive migration and MMP1 production.
  • Ben/dUev1a cooperates with Ras(V12) to promote tumor overgrowth and invasion.
  • Ben/dUev1a is required for Src42A-induced cell death and thorax closure.

Conclusions:

  • Src42A and the Ben/dUev1a complex play significant roles in developmental processes and tumor progression.
  • The study provides mechanistic insights into Src function in development and disease.
  • Mammalian Ubc13 and Uev1a may possess oncogenic functions.

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