Expression profiling by high throughput sequencing Genome binding/occupancy profiling by high throughput sequencing
Summary
Distinct lung stem cells give rise to lung adenocarcinoma (ADC) and squamous cell carcinoma (SCC). ΔNp63 guides development of these cells through regulation of terminal differentiation; however, its mechanistic role in lung cancer development has remained elusive. We utilized a ΔNp63-specific conditional knockout mouse model and found that ∆Np63 maintains lung ADC and SCC by keeping lung stem cells in quiescence. ChIP-seq analysis of lung basal cells and alveolar type 2 (AT2) cells lacking ∆Np63 revealed a robust loss of activating histone marks at super enhancers of cell identity genes defining a unifying oncogenic role for ∆Np63 in non-small cell lung cancer.
Overall design
Basal cells and AT2 cells isolated from ΔNp63fl/fl and ΔNp63Δ/Δ mice were analyzed by RNA-seq and ChIP-seq.
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