Lung cancer deficient in the tumor suppressor GATA4 is sensitive to TGFBR1 inhibition

Nat Commun. 2019 Apr 10;10(1):1665. doi: 10.1038/s41467-019-09295-7.

Abstract

Lung cancer is the leading cause of cancer-related deaths worldwide. Tumor suppressor genes remain to be systemically identified for lung cancer. Through the genome-wide screening of tumor-suppressive transcription factors, we demonstrate here that GATA4 functions as an essential tumor suppressor in lung cancer in vitro and in vivo. Ectopic GATA4 expression results in lung cancer cell senescence. Mechanistically, GATA4 upregulates multiple miRNAs targeting TGFB2 mRNA and causes ensuing WNT7B downregulation and eventually triggers cell senescence. Decreased GATA4 level in clinical specimens negatively correlates with WNT7B or TGF-β2 level and is significantly associated with poor prognosis. TGFBR1 inhibitors show synergy with existing therapeutics in treating GATA4-deficient lung cancers in genetically engineered mouse model as well as patient-derived xenograft (PDX) mouse models. Collectively, our work demonstrates that GATA4 functions as a tumor suppressor in lung cancer and targeting the TGF-β signaling provides a potential way for the treatment of GATA4-deficient lung cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • A549 Cells
  • Animals
  • Cellular Senescence / genetics
  • Down-Regulation
  • Female
  • GATA4 Transcription Factor / genetics
  • GATA4 Transcription Factor / metabolism*
  • Gene Expression Regulation, Neoplastic*
  • Gene Knockdown Techniques
  • Genes, Tumor Suppressor*
  • HEK293 Cells
  • Humans
  • Lung / pathology
  • Lung Neoplasms / drug therapy
  • Lung Neoplasms / genetics*
  • Lung Neoplasms / mortality
  • Lung Neoplasms / pathology
  • Male
  • Mice
  • Mice, Nude
  • MicroRNAs / genetics
  • MicroRNAs / metabolism
  • Middle Aged
  • Prognosis
  • Receptor, Transforming Growth Factor-beta Type I / antagonists & inhibitors
  • Receptor, Transforming Growth Factor-beta Type I / metabolism
  • Signal Transduction / genetics
  • Smad2 Protein / genetics
  • Smad2 Protein / metabolism
  • Smad4 Protein / genetics
  • Smad4 Protein / metabolism
  • Transforming Growth Factor beta2 / metabolism
  • Up-Regulation
  • Wnt Proteins / genetics
  • Wnt Proteins / metabolism*
  • Xenograft Model Antitumor Assays

Substances

  • GATA4 Transcription Factor
  • GATA4 protein, human
  • MicroRNAs
  • SMAD2 protein, human
  • SMAD4 protein, human
  • Smad2 Protein
  • Smad4 Protein
  • TGFB2 protein, human
  • Transforming Growth Factor beta2
  • WNT7B protein, human
  • Wnt Proteins
  • Receptor, Transforming Growth Factor-beta Type I
  • TGFBR1 protein, human