Misshapen disruption cooperates with rasv12 to drive tumorigenesis

Du Kong, Jin Yu Lu, Xiaoqin Li, Sihua Zhao, Wenyan Xu, Jinan Fang, Xing Wang, Xianjue Ma

Research output: Contribution to journalArticlepeer-review

1 Scopus citations


Although RAS family genes play essential roles in tumorigenesis, effective treatments targeting RAS-related tumors are lacking, partly because of an incomplete understanding of the complex signaling crosstalk within RAS-related tumors. Here, we performed a large-scale genetic screen in Drosophila eye imaginal discs and identified Misshapen (Msn) as a tumor suppressor that synergizes with oncogenic Ras (RasV12 ) to induce c-Jun N-terminal kinase (JNK) activation and Hippo inactivation, then subsequently leads to tumor overgrowth and invasion. Moreover, ectopic Msn expression activates Hippo signaling pathway and suppresses Hippo signaling disruptioninduced overgrowth. Importantly, we further found that Msn acts downstream of protocadherin Fat (Ft) to regulate Hippo signaling. Finally, we identified msn as a Yki/Sd target gene that regulates Hippo pathway in a negative feedback manner. Together, our findings identified Msn as a tumor suppressor and provide a novel insight into RAS-related tumorigenesis that may be relevant to human cancer biology.

Original languageEnglish (US)
Article number894
Issue number4
StatePublished - Apr 2021
Externally publishedYes


  • Drosophila
  • Ft
  • Hippo
  • Msn
  • Ras
  • Tumorigenesis

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


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