Nasopharyngeal carcinoma cell lines (expression analysis and copy number analysis)
Ontology highlight
ABSTRACT: This SuperSeries is composed of the following subset Series: GSE15047: Nasopharyngeal carcinoma cell lines (expression analysis) GSE15051: Nasopharyngeal carcinoma cell lines (copy number analysis) This study was designed to screen genes overexpression due to copy number gain.
Project description:Five NPC cell lines (HONE1, CNE1, CNE2, 5-8F, and 6-10B) and an immortalized nasopharyngeal epithelial cell line NP69 were evaluated with 250K SNP arrays (Affymetrix) to detect the genome-wide DNA copy number alterations. The same type of data of 45 Chinese samples from the HapMap project was used as normal control. Data was analyzed using GCOS (GeneChip operating software, Ver.1.4), GTYPE (GeneChip Genotyping Analysis Software, Ver.4.1), and CNAT (chromosome copy number analysis tool, Ver.4.0, BRLMM algorithm).
Project description:Three nasopharyngeal carcinoma cell lines (CNE1, CNE2, and HONE1) expression patterns against an immortalized nasopharyngeal epithelial cell line NP69. This study was done to screen genes consensually overexpressed in NPC. NP69 was used as normal control. The microarray analyses were done in a same batch.
Project description:High metastatic nasopharyngeal carcinoma cell line 5-8F expression patterns against low metastatic nasopharyngeal carcinoma cell line 6-10B. This study was done to screen genes related with metastasis in NPC. The microarray analyses were done in a same batch. 6-10B cells are cultured and harvested at three different time points.
Project description:High metastatic nasopharyngeal carcinoma cell line 5-8F expression patterns. This study was done to detect genes expressed in NPC cell line 5-8F. The microarray analyses were done in a same batch. cells are cultured and harvested at two different time points.
Project description:JIB-04 is an inhibitor of Jumonji histone demethylases identified through a cell based screen that measures the reactivation of an epigenetically silenced transgene. The active JIB-04 E-isomer shows selectivity for cancer vs. normal cells affecting both transcriptional patterns and cell viability in a cancer specific manner. H358 lung cancer cells or the patient matched HCC4017 (cancer) vs. HBEC30KT (immortalized normal) lung cell pair were treated with DMSO vehicle or 500nM E-isomer or 500 nM Z-isomer of JIB-04 for 4 h or 24 h and RNA extracted.
Project description:As regulators in gene expression, microRNAs take part in most biological process including cell differentiation, apoptosis, cell cycle and epithelial-to-mesenchymal transition (EMT). In order to evaluate their roles during the growth factors-induced EMT process, microRNA expression profile changes induced by EGF or TGF-β treatment on nasopharyngeal carcinoma cell line HK-1 cells were analyzed by means of the Affymetrix genome wide microarray system. Human nasopharyngeal carcinoma cell line HK-1 was starved for 12 hours before stimulation with EGF (50 ng/mL) or TGF-β (10ng/ml) or Control (PBS) for 36 hours in RPMI-1640 medium (with 1% serum) to establish the in vitro model of EMT. Total RNA were extracted and detected by Affymetrix® GeneChip® miRNA Arrays.
Project description:We utilized non-transformed, human pancreatic ductal epithelial (HPDE) cells, previously engineered with the E6 and E7 proteins of the HPV16 virus to emulate loss of p53 and inactivation of the Rb pathway, respectively. Given the frequent activation of KRAS (>90% PDAC tumors) and its early role in pancreatic neoplasia, we sought to engineer HPDE cells containing KRASG12D to provide the appropriate context in which to screen for novel drivers that might represent KRAS effectors. The KRAS-induced transcription analysis was conducted using RNAs extracted from HPDE cells transduced with either control, wild-type KRAS or KRASG12D(pInducer) with or without DOX (100ng/ml) for 72 h, followed by hybridization of labeled cDNA onto Agilent arrays (Agilent G3 Human GE 8x60K) by the Baylor College of Medicine Genome Profiling Core Facility. multi-group comparison
Project description:The elevation of guanine nucleotide binding protein alpha 12 (GM-NM-112) expression is highly associated with tumor invasiveness in several human cancers. We used an siRNA strategy to deplete GM-NM-112 in oral squamous cell carcinoma (OSCC) cells and analyze the transcriptome profile by the Affymetrix Human Exon 1.0 ST platform. Transcriptome analysis of total RNA samples from OSCC cells. We analyzed OSCC cell samples using the Affymetrix Human Exon 1.0 ST platform. Array data was processed by the Affymetrix Exon Array Computational Tool. No technical replicates were performed.
Project description:In diabetics, methylglyoxal (MG), a glucose-derived metabolite, plays a noxious role by inducing oxidative stress, which causes and exacerbates a series of complications. With the use of microarray analysis, we comprehensively screened the gene expression profiles of ST2 cells, derived from a multipotent bone marrow stromal cell line, in the presence or absence of oxidative stress induced by100 M-NM-<M methylglyoxal (MG) treatment to charactrize genes related to diabetic complications. Mouse bone marrow stromal cell-line ST2 (RIKEN, Tsukuba, Japan) was cultured in M-NM-1-MEM (Sigma, St. Louis, MO) supplemented with 10% FBS (Sigma), 100 M-NM-<g/ ml penicillin/ streptomycin (ICN Biomedicals, Inc., Aurora, OH) and 100 M-NM-<M methylglyoxal (MG), and maintained at 37M-BM-0C in a humidified atmosphere with 5% CO2. Total RNA was isolated from ST2 cells treated with or without 100 M-NM-<M methylglyoxal (MG) or 1 M-NM-<M of 5-aza-2M-bM-^@M-^Y-deoxycytidine (5-aza-dC) by standard methods with the use of an RNeasy Protect Mini kit (Qiagen KK, Tokyo, Japan) according to the manufacturerM-bM-^@M-^Ys instructions. Cy3, Cy5 differential expression asasy by Mouse 32K Filgen array
Project description:Humanin (HN) is a 24 amino acid peptide encoded by mitochondrial DNA MT-RNR2 (16S ribosomal RNA [rRNA]). It was previously shown, that HN protects tumor cells from damage during chemotherapy. To get mechanistic insight of HN induced singaling cascades involved in brain tumor growth, we performed a global phosphoproteomic analysis total and phosphorylated proteins on human brain tumor cells after treatment with the peptide Humanin.