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PTEN regulates lung endodermal morphogenesis through MEK/ERK pathway

Yiming Xing1, Runming Wang1, Changgong Li2

  • 1The State Key Laboratory for Agro-biotechnology, China Agricultural University, Beijing 100191, PR China.

Developmental Biology
|October 14, 2015
PubMed

Insights

Loss of the Pten gene in embryonic lungs disrupts branching and cell migration. This process appears to involve the ERK signaling pathway, but not AKT, highlighting Pten

Area of Science:

  • Developmental Biology
  • Cancer Research
  • Cell Signaling

Background:

  • The phosphatase and tensin homolog (Pten) gene is a crucial tumor suppressor involved in various cellular functions.
  • Pten mutations are linked to numerous human cancers.
  • Pten's role in cell migration and its precise mechanism in lung development are not fully understood.

Purpose of the Study:

  • To investigate the function of Pten in embryonic lung branching morphogenesis.
  • To elucidate the specific signaling pathways, particularly ERK and AKT, involved in Pten-mediated lung development.

Main Methods:

  • Conditional deletion of Pten in embryonic lung epithelium using Gata5-cre mice.
  • Analysis of branching morphogenesis, cell proliferation, and cell migration in Pten-deficient lungs.
  • Utilizing explant models and conditional mutants to block ERK or AKT phosphorylation.

Main Results:

  • Pten deletion blocked embryonic lung branching and phosphorylation of ERK and AKT.
  • Pten-deficient lung endoderm explants failed to branch, with disrupted cell migration but unaffected proliferation.
  • Blocking ERK phosphorylation, but not AKT, exacerbated the branching defect, implicating ERK in Pten's role.

Conclusions:

  • Pten is essential for embryonic lung branching morphogenesis.
  • Pten's requirement for lung development involves regulating cell migration.
  • The ERK signaling pathway, not AKT, mediates Pten's role in embryonic lung endodermal morphogenesis and cell migration.
Keywords:
AKTBranching morphogenesisCell migrationERKEndodermLung morphogenesisPten

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