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Tumor Allotransplantation in Drosophila melanogaster with a Programmable Auto-Nanoliter Injector
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Two-Faced: Roles of JNK Signalling During Tumourigenesis in the Drosophila Model

John E La Marca1, Helena E Richardson1

  • 1Richardson Laboratory, Department of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, VIC, Australia.

Frontiers in Cell and Developmental Biology
|March 3, 2020
PubMed

Insights

The c-Jun N-terminal Kinase (JNK) pathway in Drosophila melanogaster plays dual roles in tumor development, acting as both a tumor suppressor and promoter. Its context-dependent functions are crucial for understanding cancer progression.

Area of Science:

  • Cellular signaling pathways
  • Developmental biology
  • Cancer research

Background:

  • The c-Jun N-terminal Kinase (JNK) signaling pathway is highly conserved and regulates diverse cellular processes.
  • JNK signaling has context-dependent roles in tumor development, acting as both a tumor suppressor and promoter.
  • JNK pathway activation can be triggered by various stimuli, including TNF signaling, actin cytoskeleton alterations, and reactive oxygen species (ROS).

Purpose of the Study:

  • To review the multifaceted roles of JNK signaling in Drosophila melanogaster tumor models.
  • To highlight recent findings on JNK's involvement in tumor suppression and promotion.
  • To discuss JNK's interactions with other signaling pathways, such as Salvador-Warts-Hippo (SWH) and Ras-MAPK.

Main Methods:

  • Review of existing literature on JNK signaling in Drosophila tumor models.
  • Analysis of studies investigating JNK's pro- and anti-tumorigenic functions.
  • Examination of JNK's interactions with other signaling pathways and its non-autonomous effects.

Main Results:

  • JNK signaling acts as a tumor suppressor when activated by TNF signaling, promoting caspase-mediated cell death.
  • JNK signaling promotes tumorigenesis by driving cell morphology changes, invasion, blocking differentiation, and enabling proliferation, often in concert with Ras-MAPK.
  • JNK signaling influences tumor microenvironments through non-autonomous effects on growth-promoting molecules.

Conclusions:

  • JNK signaling exhibits complex and context-dependent roles in Drosophila tumorigenesis.
  • Understanding JNK's dual functions is critical for developing targeted cancer therapies.
  • Further research is needed to fully elucidate the intricate mechanisms of JNK signaling in cancer.
Keywords:
DrosophilaJNKRasapoptosisscribtumourigenesis

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