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Role and regulation of Yap in KrasG12D-induced lung cancer

Yaopan Mao1, Shuguo Sun1,1, Kenneth D Irvine1

  • 1Waksman Institute, Cancer Institute of New Jersey, Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, NJ 08854, USA.

Oncotarget
|January 18, 2018
PubMed

Insights

The Hippo pathway

Area of Science:

  • Oncology
  • Molecular Biology

Background:

  • The Hippo pathway and its downstream transcriptional co-activator Yap are implicated in lung cancer.
  • The precise role of Yap in lung tumorigenesis remains incompletely understood.

Purpose of the Study:

  • To elucidate the role of Yap in KrasG12D and p53 loss-driven lung adenocarcinoma initiation and progression.
  • To characterize Yap expression patterns during lung tumor development.

Main Methods:

  • Utilized a genetically engineered mouse model of lung cancer.
  • Investigated the effects of Yap deletion and heterozygosity on tumor initiation and progression.
  • Analyzed Yap expression levels at various stages of tumorigenesis.

Main Results:

  • Complete Yap deletion abolished KrasG12D and p53 loss-driven lung adenocarcinoma initiation and progression.
  • Partial Yap suppression (heterozygosity) partially inhibited lung cancer growth.
  • Nuclear Yap was detected early in lung carcinogenesis, with levels correlating with proliferation in later stages.

Conclusions:

  • Yap is essential for KrasG12D and p53 loss-driven lung tumorigenesis, despite not being directly activated by oncogenic Kras.
  • Yap represents a potential therapeutic target for lung adenocarcinoma.
Keywords:
KrasYAPadenocarcinomalung cancer

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