ArticleOncogene2020
Tumor progression and chromatin landscape of lung cancer are regulated by the lineage factor GATA6.
Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Article
- From Transcription Factors Dysregulation to Malignancy: In Silico Reconstruction of Cancer's Foundational Drivers-The Eternity Triangle.International journal of molecular sciences · 2025Article
- Single-cell transcriptomics reveals the multidimensional dynamic heterogeneity from primary to metastatic gastric cancer.iScience · 2025Article
- Theoretical perspectives and clinical applications of non-coding RNA in lung cancer metastasis: a systematic review.Discover oncology · 2025Review
- GATA6 inhibits the biological function of non-small cell lung cancer by modulating glucose metabolism.Journal of cancer research and clinical oncology · 2024Article
- Distinct fibroblast subpopulations associated with bone, brain or intrapulmonary metastasis in advanced non-small-cell lung cancer.Clinical and translational medicine · 2024Article
- Preliminary results from the EMoLung clinical study showing early lung cancer detection by the LC score.Discover oncology · 2023Article
- Article
- Article
- Long non-coding RNA GATA6-AS1 upregulates GATA6 to regulate the biological behaviors of lung adenocarcinoma cells.BMC pulmonary medicine · 2021Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Lineage selective transcription factors (TFs) are important regulators of tumorigenesis, but their biological functions are often context dependent with undefined epigenetic mechanisms of action. In this study, we uncover a conditional role for the endodermal and pulmonary specifying TF GATA6 in lung adenocarcinoma (LUAD) progression. Impairing Gata6 in genetically engineered mouse models reduces the proliferation and increases the differentiation of Kras mutant LUAD tumors. These effects are influenced by the epithelial cell type that is targeted for transformation and genetic context of Kras-mediated tumor initiation. In LUAD cells derived from surfactant protein C expressing progenitors, we identify multiple genomic loci that are bound by GATA6. Moreover, suppression of Gata6 in these cells significantly alters chromatin accessibility, particularly at distal enhancer elements. Analogous to its paradoxical activity in lung development, GATA6 expression fluctuates during different stages of LUAD progression and can epigenetically control diverse transcriptional programs associated with bone morphogenetic protein signaling, alveolar specification, and tumor suppression. These findings reveal how GATA6 can modulate the chromatin landscape of lung cancer cells to control their proliferation and divergent lineage dependencies during tumor progression.
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