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Gene expression profiling of WT and Aldh1a1 KO mouse lung tissues exposed to naphthalene

ABSTRACT: Gene expression profiling of WT and Aldh1a1 KO mouse lung tissues exposed to naphthalene

PROVIDER: PRJNA1212218 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32039436.fastq.gz	Fastqsanger.gz
	SRR32039437.fastq.gz	Fastqsanger.gz
	SRR32039438.fastq.gz	Fastqsanger.gz
	SRR32039439.fastq.gz	Fastqsanger.gz

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Gene expression profiling of WT and Aldh1a1 KO mouse lung tissues exposed to naphthalene

Project description:To explore potential impact of Aldh1a1 deficiency in the retinoic acid signaling in the lung, gene expression levels were compared between wildtype and Aldh1a1 deficient lung tissues. The expression levels of retinoic acid responsive genes were very similar between wildtype and Aldh1a1 deficient lungs, suggesting that Aldh1a1 deficiency has minimal impact on retinoic acid signaling.

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Gene expression profiling of WT and Aldh1a1 KO mouse lung tissues

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Gene expression profiling of WT and Aldh1a1 KO mouse lung tissues

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Effect of naphthalene on gene expression of C57BL/6J mouse lung cells

Project description:Transcriptomic analysis on naphthalene exposed mouse lung cells was performed to discover molecular biomarkers for environmental toxin responses in respiratory orgnas. DEG analysis revelaed 293 genes with significant expression changes in naphthalene treated samples. GO enrichment analysis result showed GO terms related to cillum, axoneme and dynein complex were enriched in down-regulated genes and stress response terms in up-regulated genes. These results indicate when exposed to naphthalene, genes with increased expression levels are associated with chemical response and inflammation, while genes with decreased expression levels are associated with pseudostratified epithelical cells in respiratory organ.

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Loss of ARID1A induces a stemness gene ALDH1A1 expression with histone acetylation in the malignant subtype of cholangiocarcinoma

Project description:Genomic analyses have recently discovered the malignant subtype of human intrahepatic cholangiocarcinoma (ICC) characterized by frequent mutations of chromatin remodeling gene ARID1A, however, the biological and molecular functions still remain obscure. We here examined the clinical and biological significances of ARID1A deficiency in human ICC. Immunohistochemical analysis demonstrated that loss of ARID1A was an independent prognostic factor for overall survival of ICC patients (P = 0.023). We established ARID1A-knockout (KO) cells by using the CRISPR/Cas9 system from two human cholangiocarcinoma cell lines. ARID1A-KO cells significantly enhanced migration, invasion, and sphere formation activity. Microarray analysis revealed that ALDH1A1, a stemness gene, was the most significantly elevated genes in ARID1A-KO cells. In addition, ALDH enzymatic activity as a hallmark of cancer stem cells was markedly high in the KO cells. ARID1A and histone deacetylase 1 directly recruited to the ALDH1A1 promoter region in cholangiocarcinoma cells with undetectable ALDH1A expression by chromatin immunoprecipitation assay. The histone H3K27 acetylation level at the ALDH1A1 promoter region was increased in cells when ARID1A was disrupted (P < 0.01). Clinically, inverse correlation between ARID1A and ALDH1A expression was also detected in primary ICC (P = 0.018), and ARID1A-negative and ALDH1A1-positve ICCs showed worse prognosis than only ARID1A-negative cases (P = 0.002). In conclusion, ARID1A may function as a tumor suppressor in ICC through transcriptional down-regulation of ALDH1A1 expression with decreasing histone H3K27 acetylation. Our studies provide the basis for the development of new epigenetic approaches to ARID1A-negative ICC.

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