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Updated: Nov 7, 2025

Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia
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Published on: July 25, 2017

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Misshapen Disruption Cooperates with Ras to Drive Tumorigenesis

Du Kong1,2,3,4, Jin-Yu Lu5, Xiaoqin Li6,7

  • 1School of Medicine, Zhejiang University, Hangzhou 310058, China.

Cells
|April 30, 2021
PubMed

Insights

Misshapen (Msn) acts as a tumor suppressor by interacting with Ras signaling to control cell growth. This study uncovers Msn

Area of Science:

  • Cell Biology
  • Genetics
  • Cancer Research

Background:

  • RAS family genes are crucial in tumorigenesis.
  • Effective treatments for RAS-related tumors are limited due to complex signaling crosstalk.
  • Understanding these pathways is vital for cancer therapy.

Purpose of the Study:

  • To identify novel tumor suppressors involved in RAS-related tumorigenesis.
  • To elucidate the role of Misshapen (Msn) in regulating cell growth and invasion.
  • To investigate the interplay between Msn, Ras, and the Hippo signaling pathway.

Main Methods:

  • Large-scale genetic screen in Drosophila eye imaginal discs.
  • Analysis of c-Jun N-terminal kinase (JNK) activation and Hippo signaling.
  • Investigated the regulatory relationship between Msn, Fat (Ft), and Hippo signaling.

Main Results:

  • Misshapen (Msn) was identified as a tumor suppressor that synergizes with oncogenic Ras.
  • Msn induces JNK activation and Hippo inactivation, promoting tumor overgrowth and invasion.
  • Msn acts downstream of Fat (Ft) and is a target of Yki/Sd, regulating the Hippo pathway in a negative feedback loop.

Conclusions:

  • Msn functions as a tumor suppressor in the context of Ras-driven tumorigenesis.
  • Msn plays a critical role in regulating the Hippo signaling pathway.
  • These findings offer novel insights into RAS-related tumorigenesis with potential relevance to human cancers.
Keywords:
DrosophilaFtHippoMsnRastumorigenesis

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