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Genome-wide tongue epithelia transcriptomic profiles from K14-rtTA;TRE-FLBmi-1 + 4-nitroquinoline 1-oxide (4-NQO), 25 weeks (KrTB-N (25w)), KrTB+Doxycycline+4-NQO, 4 weeks (KrTB-DN (4w)), and KrTB+Doxycycline+4-NQO, 10 weeks (KrTB-DN (10w)).

ABSTRACT: 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 stem cells (SCs) of the tongue. Here we used this transgenic mouse line to delineate BMI1 actions in early-stage oral squamous cell carcinoma (OSCC). We observed more oncogenic changes in mice with ectopic BMI1 expression after 4 weeks of 4-nitroquinoline 1-oxide (4-NQO) treatment. We detected increased proliferation and oxidative stress, as well as increased expression of multiple transcripts and proteins linked to human OSCCs, in murine tongue epithelia with high BMI1 expression during early carcinogen-induced tumorigenesis. Furthermore, increases in mRNAs encoding multiple metabolic targets, such as SLC16A3, PKM, and GPI1, were accelerated upon BMI1 overexpression in our 4-NQO model.

ORGANISM(S): Mus musculus

PROVIDER: GSE307391 | GEO | 2025/12/09

REPOSITORIES: GEO

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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).

Project description: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.

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2014-07-01 | E-GEOD-54246 | biostudies-arrayexpress

Genome-wide tongue epithelia transcriptomic profiles from K14-rtTA TRE-FLBmi-1 + 4-nitroquinoline 1-oxide (4-NQO), 25 weeks (KrTB-N (25w)), KrTB+Doxycycline+4-NQO, 4 weeks (KrTB-DN (4w)), and KrTB+Doxycycline+4-NQO, 10 weeks (KrTB-DN (10w)).

Project description:Genome-wide tongue epithelia transcriptomic profiles from K14-rtTA TRE-FLBmi-1 + 4-nitroquinoline 1-oxide (4-NQO), 25 weeks (KrTB-N (25w)), KrTB+Doxycycline+4-NQO, 4 weeks (KrTB-DN (4w)), and KrTB+Doxycycline+4-NQO, 10 weeks (KrTB-DN (10w)).

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Genome-wide tongue epithelia transcriptomic profiles from K14-rtTA;TRE-FLBmi-1 (KrTB) and KrTB+Doxycycline (KrTB+DOX).

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Transcription profiling of mouse lymphoma L5178Y cells treated with 4-NitroQuinoline N-Oxide (4-NQO) ILSI-HESI Genotoxicity Study - 4-NQO

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Effect of deletion of Sisfha on gene expression of Saccharolobus islandicus REY15A in the presence of 4-nitroquinoline 1-oxide (NQO)

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Molecular characterization of 4-NQO induced F344 rat tongue carcinogenesis: alteration of multiple gene expression and hypomethylation of PTGS2 proximal promoter

Project description:The 4-NQO induced rat tongue carcinogenesis model presenting considerable histologic and molecular similarity to oral cancers commonly seen in humans is very useful for investigating oral carcinogenesis. In order to understand the molecular basis of oral carcinogenesis and identify gene biomarkers and potential chemopreventive targets for future studies, we characterized the molecular changes in oral squamous cell carcinoma (SCC) samples generated from this model system using F344 rats by performing gene expression microarray and methylation analysis of selected genes. Microarray studies identified 1735 genes to be upregulated by at least 2 fold (p<0.05, n=11) and 1803 genes to be downregulated by at least 50% (p<0.05, n=11) in SCC in comparison to the adjacent normal tissues and 28 KEGG pathways to be altered in SCC (p<0.01). Among the altered genes, keratins and keratin associated proteins were found to be differentially regulated and the keratin profile appeared to an important biomarker for oral SCC. PTGS2 and PTGS2 relevant genes, which are potential targets of chemoprevention and therapy, were also found to be upregulated in SCC and confirmed by qRT-PCR. The upregulation of PTGS2 appeared to correlate with hypomethylation of its proximal promoter. Methylation analysis of other selected genes showed that the first exon of APC2 was methylated in normal tissues, and the methylation level increased moderately in SCC samples (p<0.01, n=8). These results demonstrate that 4-NQO induced tongue carcinogenesis in F344 rats is accompanied by alteration of multiple gene expression, hypomethylation of PTGS2 and increased methylation of APC2. Gene expression in untreated normal vs.4-NQO induced tongue tumors in F344 rats (n=11).

2014-08-04 | E-GEOD-51125 | biostudies-arrayexpress

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