Genetic and pharmacologic disruption of N-Myc suppresses basal cell carcinoma [RNA-seq]

Here, we performed spatial transcriptomics to show that nascent murine BCC-like tumors are comprised of two tumor sub-populations that differ in expression of Hh, stem cell and differentiation markers.

Using a newly developed cell culture formulation termed “RRi conditions,” we established several mouse BCC cell lines, identify novel genes associated with Hh pathway activation (Wnt7b, Tgfb3, Cxcl14), and show that inducible N-MYC expression suppresses Notch signaling and Krt10, a canonical squamous differentiation marker. Furthermore, we report that genetically ablating N-Myc slows tumor initiation and progression, and that an immunomodulatory drug, imiquimod, can suppress N-Myc and regress nascent lesions.