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Rounding up the Usual Suspects: Assessing Yorkie, AP-1, and Stat Coactivation in Tumorigenesis

Fisun Hamaratoglu1, Mardelle Atkins2

  • 1School of Biosciences, Cardiff University, CF103AX, Cardiff, UK.

International Journal of Molecular Sciences
|July 2, 2020
PubMed

Insights

Hyperactivation of key signaling pathways like Jun N-terminal Kinase (JNK), Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT), and Hippo may drive most epithelial cancers. These pathways, along with Notch signaling, are commonly deregulated across various tumor models.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Epithelial cancers arise from diverse driver mutations.
  • Identifying common underlying mechanisms is crucial for effective cancer therapies.
  • Signaling pathway hyperactivation is a potential unifying factor.

Purpose of the Study:

  • To investigate if hyperactivation of specific signaling pathways drives most epithelial cancers.
  • To analyze gene expression and pathway activity in Drosophila tumor models.
  • To identify commonly deregulated pathways across different cancer types.

Main Methods:

  • Utilized Drosophila tumor models with known initiating mutations.
  • Analyzed transcriptomic data to evaluate activity levels of eight signaling pathways.
  • Assessed the roles of Jun N-terminal Kinase (JNK), Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT), and Hippo pathways.

Main Results:

  • At least two of the three suspect pathways (JNK, JAK/STAT, Hippo) contributed to tumor development in all assessed Drosophila cancer models.
  • Notch signaling was found to be globally activated in all examined models.
  • Pathway deregulation was observed irrespective of initiating mutations or tissue of origin.

Conclusions:

  • The JNK, JAK/STAT, Hippo, and Notch signaling pathways are frequently and globally deregulated in epithelial cancers.
  • These four pathways represent promising targets for systematic investigation and therapeutic development.
  • Targeting these common pathways could offer a unified strategy for treating a majority of epithelial cancers.
Keywords:
DrosophilaHippoJAK/STATJNKNotchcancersignaling

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