ArticleDevelopmental cell2022
FoxA1 and FoxA2 control growth and cellular identity in NKX2-1-positive lung adenocarcinoma.
Article in Developmental cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 52 citations in OpenAlex.
- Mutant p53 sensitizes KRAS-driven lung adenocarcinoma to immunotherapy by repressing SPP1.Science advances · 2026Article
- Systemic Molecular Network Alterations Associated with FoxA2 in Gastric Cancer.International journal of molecular sciences · 2026Article
- HNF4α controls growth, identity, and KRAS inhibitor response in invasive mucinous adenocarcinoma of the lung.The Journal of clinical investigation · 2026Article
- KMT2D loss drives adeno-to-squamous transition and sensitizes TKI-resistant lung cancer to AURKA inhibition.Cell death and differentiation · 2026Article
- The role of HNF4α in adenocarcinoma.Biochemical Society transactions · 2026Review
- FOXA2 promotes the occurrence and development of osteosarcoma cells by regulating ferroptosis through the Rheb/mTOR axis.World journal of surgical oncology · 2026Article
- FOXA2 in cancer: from fundamental biology to clinical translation.Frontiers in oncology · 2026Review
- Evolution of Cancer Metastases via Lineage Trans-Differentiation.Research (Washington, D.C.) · 2026Article
- Article
- Long Non-Coding RNAs Contribute to Glucose Starvation-Induced Dedifferentiation in Lung Adenocarcinoma.Biomolecules · 2025Article
- Tumor mutational burden, gene expression patterns, and immune-cell deconvolution in testicular germ cell tumors.Translational andrology and urology · 2025Article
- Panorama of Chromosomal Instability in Lung Cancer.medRxiv : the preprint server for health sciences · 2025Article
- Lineage rewiring in lung adenocarcinoma via HNF4α and NKX2-1 dynamics.Genes & development · 2025Article
- Opposing lineage specifiers induce a protumor hybrid identity state in lung adenocarcinoma.Genes & development · 2025Article
- NKX2-1 Restricts the Growth and Metastasis of Lung Squamous Cell Carcinoma Through Transcriptive Suppression of AKR1B10.Journal of biochemical and molecular toxicology · 2025Article
- Persistent lineage plasticity driving lung cancer development and progression.Clinical and translational medicine · 2025Review
- Relationship Between Activating Transcription Factor 3 and Forkhead Box Protein A2 in Spinal Cord Injury and the Underlying Mechanism.Applied biochemistry and biotechnology · 2025Article
- NKX2-1 drives neuroendocrine transdifferentiation of prostate cancer via epigenetic and 3D chromatin remodeling.Nature genetics · 2025Article
- Amplified dosage of the NKX2-1 lineage transcription factor controls its oncogenic role in lung adenocarcinoma.Molecular cell · 2025Article
- Pan-cancer genomic analysis reveals FOXA1 amplification is associated with adverse outcomes in non-small cell lung, prostate, and breast cancers.Journal of the National Cancer Institute · 2025Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Changes in cellular identity (also known as histologic transformation or lineage plasticity) can drive malignant progression and resistance to therapy in many cancers, including lung adenocarcinoma (LUAD). The lineage-specifying transcription factors FoxA1 and FoxA2 (FoxA1/2) control identity in NKX2-1/TTF1-negative LUAD. However, their role in NKX2-1-positive LUAD has not been systematically investigated. We find that Foxa1/2 knockout severely impairs tumorigenesis in KRAS-driven genetically engineered mouse models and human cell lines. Loss of FoxA1/2 leads to the collapse of a dual-identity state, marked by co-expression of pulmonary and gastrointestinal transcriptional programs, which has been implicated in LUAD progression. Mechanistically, FoxA1/2 loss leads to aberrant NKX2-1 activity and genomic localization, which in turn actively inhibits tumorigenesis and drives alternative cellular identity programs that are associated with non-proliferative states. This work demonstrates that FoxA1/2 expression is a lineage-specific vulnerability in NKX2-1-positive LUAD and identifies mechanisms of response and resistance to targeting FoxA1/2 in this disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.