Project description:cAMP responsive element binding protein 1 (CREB1) is a transcription factor belonging to the basic leucine zipper (bZIP) family. Previous studies on the transcriptional regulatory targets of CREB1 have focused on protein-coding genes. The non-coding targets regulated by CREB1 in gastric cancer remain to be further studied. Herein, the genome-wide mapping of CREB1 binding in gastric cancer cell AGS was determined by chromatin immunoprecipitation sequencing.
Project description:Long noncoding RNAs (LncRNAs) are an important class if pervasive genes involved in a variety of biological functions. LncRNAs have been recently implicated as having oncogenic and tumor suppressor roles. To further investigate the function of lncRNA in gastric cancer, we use lncRNA microarray to describe LncRNAs profiles in 6 pairs of human gastric adenocarcinoma and the corresponding adjacent nontumorous tissues. The experimental samples are divided into two groups(normal and tumor) to compare lncRNA expression profiling of those
Project description:Long noncoding RNAs (LncRNAs) are an important class if pervasive genes involved in a variety of biological functions. LncRNAs have been recently implicated as having oncogenic and tumor suppressor roles. To further investigate the function of lncRNA in gastric cancer, we use lncRNA microarray to describe LncRNAs profiles in 6 pairs of human gastric adenocarcinoma and the corresponding adjacent nontumorous tissues.
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this work is comprehensive analysis of target genes co-regulated by CREB1 and FoxA1 in prostate cancer cell models, tissues, and circulating tumor cells (CTCs). Expression of CREB1/FoxA1 target genes corresponds with disease recurrence and aggressive clinical features. Methods: LNCaP cells between passage number 32-34 and abl between 62-64 were used for assay. For RNA-seq, cells are transfected with FoxA1,CREB1 specific or nonspecific siRNA and total RNA is extracted with Qiangen RNeasy Mini kit(cat 74104) and library is generated with TruSeq RNA Sample Preparation Kit v2 from Illumina(cat RS-122-2001). For Chip-seq, LNCaP cells between passage number 32-34 and abl between 62-64 were used for assay. After crosslinking with 1% formaldehyde, ChIP was performed. the ChIP producted was further used to generate library with illumina ChIP-seq kit. Hi-seq 2500 was used for sequencing and the data was analyzed by MACs for peaks. LNCaP cells and LNCaP cells were used as cell model. Library was sequenced using Illumina HISeq 2500.
Project description:Copy number profiling of 27 gastric cancer cell lines and 105 gastric tumor tissues. we hypothesized that a detailed fine-scale survey of genomic CNAs might reveal potential genes disrupted by fusion events in gastric cancer. We inferred the locations of likely chromosomal breakpoints by identifying regions where closely-spaced microarray probes exhibited striking transitions in copy number. 27 gastric cancer cell lines and 105 gastric tumor tissues were profiled by Agilent 244K microarray.
Project description:Exosomes from the culture media (CM) of four GC cells (GCCs) and human gastric epithelial cells were isolated. Exosomal RNA was extracted, and lncRNA microarray assay was performed to identify GC-specific exosomal lncRNAs. A total of 199 exosomal lncRNAs were expressed at considerable higher levels in GCCs than those in normal controls, among which the top 10 upregulated lncRNAs were selected for further validation. qRT-PCR revealed that lnc-SLC2A12-10:1 was remarkably upregulated in exosomes derived from patients with GC and GCCs. The expression levels of the candidate exosomal lncRNAs lnc-SLC2A12-10:1 were validated in 120 subjects via quantitative reverse transcription PCR (qRT-PCR).The result suggested that exosomal lnc-SLC2A12-10:1 may be a potential noninvasive biomarker for the diagnosis and prognosis monitoring of GC.
Project description:Copy number profiling of 27 gastric cancer cell lines and 105 gastric tumor tissues. we hypothesized that a detailed fine-scale survey of genomic CNAs might reveal potential genes disrupted by fusion events in gastric cancer. We inferred the locations of likely chromosomal breakpoints by identifying regions where closely-spaced microarray probes exhibited striking transitions in copy number.
Project description:Background: Exceptional and extreme feeding behaviour makes the Burmese python (Python bivittatus) an interesting model to study physiological remodelling and metabolic adaptation in response to refeeding after prolonged starvation. In this study, we used transcriptome sequencing of five visceral organs during fasting as well as 24h and 48h after ingestion of a large meal to unravel the postprandial changes in Burmese pythons. We first used the pooled data to perform a de novo assembly of the transcriptome and supplemented this with a proteomic survey of enzymes in the plasma and gastric fluid. Results: We constructed a high-quality transcriptome with 34,423 transcripts of which 19,713 (57%) were annotated. Among highly expressed genes (FPKM>100 in one tissue) we found the transition from fasting to digestion was associated with differential expression of 43 genes in the heart, 206 genes in the liver, 114 genes in the stomach, 89 genes in the pancreas and 158 genes in the intestine. We interrogated the function of these genes to test previous hypotheses on the response to feeding. We also used the transcriptome to identify 314 secreted proteins in the gastric fluid of the python Conclusions: Digestion was associated with an upregulation of genes related to metabolic processes, and translational changes therefore appears to support the postprandial rise in metabolism. We identify stomach-related proteins from a digesting individual and demonstrate that the sensitivity of modern LC-MS/MS equipment allows the identification of gastric juice proteins that are present during digestion.
Project description:To screen the genes and pathways regulated by CREB1 in the THP1 monocytes induced by LPS, THP1 monocytes were transfected by CREB1 shRNA and then treated by LPS for 3 hours.