Genome-wide tongue epithelia transcriptomic profiles from K14-rtTA;TRE-FLBmi-1 (KrTB), KrTB+Doxycycline (KrTB-D), KrTB+4-nitroquinoline 1-oxide (KrTB-N), and KrTB+Doxycycline+4-nitroquinoline 1-oxide (KrTB-DN).

We developed a transgenic mouse model (truncated K14-rtTA; TRE/Bmi1, KrTB) containing a doxycycline- (dox) controlled, Tet-responsive element system to selectively overexpress BMI1 only in the basal epithelial SCs of the tongue. Here, we used this model to delineate BMI1 actions in tongue epithelia during oral tumorigenesis (as induced by 4-nitroquinoline 1-oxide, 4-NQO). Genome-wide transcriptomics indicated that mRNAs associated with human OSCC, including SOX9, HIF1A, MMP9, INHBB, and MYOF, were further increased by ectopic BMI1 expression in murine tongue epithelia. mRNAs encoding multiple metabolic targets, such as SLC2A1 (GLUT1), PKM, LDHA, and HK2, were also increased upon BMI1 overexpression in 4-NQO-treated tongue epithelia. Overall design: Examination of genome-wide transcript levels in mouse tongue epithelia samples. 16 samples were analyzed, 4 biological replicates per condition (KrTB vs. KrTB-D and KrTB-N vs. KrTB-DN).