Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Gene expression profiling of oral cancer cell lines with or without AzC treatment

ABSTRACT: To genome-wide screening for the genes whose expression are responsible for the promoter DNA methylation, we performed the cDNA microarray with oral cancer cells before and after a DNA methyltransferase inhibitor, 5-aza-2’-deoxycytidine (AzC), treatment. Total RNA was collected from four oral cancer cell lines before or after AzC treatment.

ORGANISM(S): Homo sapiens

SUBMITTER: Chia Lee

PROVIDER: E-GEOD-38823 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

LRIG1 modulates aggressiveness of head and neck cancers by regulating EGFR-MAPK-SPHK1 signaling and extracellular matrix remodeling.

Sheu J J-C JJ Lee C-C CC Hua C-H CH Li C-I CI Lai M-T MT Lee S-C SC Cheng J J Chen C-M CM Chan C C Chao S C-C SC Chen J-Y JY Chang J-Y JY Lee C-H CH

Oncogene 20130429 11

EGFR overexpression and chromosome 3p deletion are two frequent events in head and neck cancers. We previously mapped the smallest region of recurrent copy-number loss at 3p12.2-p14.1. LRIG1, a negative regulator of EGFR, was found at 3p14, and its copy-number loss correlated with poor clinical outcome. Inducible expression of LRIG1 in head and neck cancer TW01 cells, a line with low LRIG1 levels, suppressed cell proliferation in vitro and tumor growth in vivo. Gene expression profiling, quantit ...[more]

PMID: 23624915

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Project description:Human embryonal carcinoma (EC) cells are the stem cells of nonseminoma testicular germ cells tumors (TGCTs) and share remarkable similarities to human embryonic stem (ES) cells. In prior work we found that EC cells are hypersensitive to low nanomolar doses of 5-aza deoxycytidine (5-aza) and that this hypersensitivity partially depended on unusually high levels of the DNA methyltransferase, DNMT3B. We show here that low-dose 5-aza treatment results in DNA damage and induction of p53 in NT2/D1 cells. In addition, low-dose 5-aza results in global and gene specific promoter DNA hypomethylation. Low-dose 5-aza induces a p53 transcriptional signature distinct from that induced with cisplatin in NT2/D1 cells and also uniquely downregulates genes associated with pluripotency including NANOG, SOX2, GDF3 and Myc target genes. Changes in the p53 and pluripotency signatures with 5-aza were to a large extent dependent on high levels of DNMT3B. In contrast to the majority of p53 target genes upregulated by 5-aza that did not show DNA hypomethylation, several other genes induced with 5-aza had corresponding decreases in promoter methylation. These genes include RIN1, SOX15, GPER, and TLR4 and are novel candidate tumors suppressors in TGCTs. Our studies suggest that the hypersensitivity of NT2/D1 cells to low-dose 5-aza is multifactorial and involves the combined activation of p53 targets, repression of pluripotency genes, and activation of genes repressed by DNA methylation. Low-dose 5-aza therapy may be a general strategy to treat those tumors that are sustained by cells with embryonic stem-like properties. Total RNA obtained from wild-type NT2/D1 cells treated with vehicle (control) or 10 nM 5-aza deoxycytidine for 1 day (1day) or 10 nM 5-aza deoxycytidine for 3 days (3day) or treated with 0.5 uM cisplatin (cispl) for 6 hours followed by a 24 hour recovery before harvest. Four groups in biological triplicate for total of 12 hybridizations on Illumina HT-12v4 beadarray.

Dataset Information

Gene expression profiling of oral cancer cell lines with or without AzC treatment

Publications

LRIG1 modulates aggressiveness of head and neck cancers by regulating EGFR-MAPK-SPHK1 signaling and extracellular matrix remodeling.

Similar Datasets

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