Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA328264 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genome-wide mRNA expression profiling was performed in AGS, gastric cancer cell line, upon miR-25 silencing. At 48 hours upon anti-miR-25-3p (miRNA inhibitor) and non-targeting control RNA transfection, the whole transcriptome profiling was performed in triplicates. The miR-25 silencing elevates the diffuse gastric cancer features like expression of COL1A2, expression of COL1A2 co-expressed genes, Epithelial to Mesenchymal Transition (EMT) and angiogenesis associated genes.
2016-12-07 | GSE84196 | GEO
Project description:[Aim] EBVaGC accounts for about 10% of gastric cancer and has a better prognosis than EBVnGC, but its molecular mechanism is still unclear. We investigated the role of EBV-miR-BART1-3p in the occurrence and development of EBVaGC by applying bioinformatics methods, high-throughput sequencing, in vitro experiments, target gene screening and verification, differential gene protein interaction network and gene regulatory network construction. [Materials and Methods] The data set GSE51575 was normalized, and the outlier samples were deleted. Finally, gene expression profiles of 11 EBVaGC and 14 EBVnGC tumor tissues and non-tumor control tissues were obtained. Differential gene function analysis was performed, and molecular regulatory network was constructed. The mRNA expression levels of SNU-719 (EBV-positive gastric cancer cell line), AGS, AGS-NC (EBV-negative gastric cancer cell line) and AGS-OE (lentivirus-transfected miR-BART1-3p overexpression cell line) were detected by high-throughput next-generation sequencing technology, and differential gene expression characteristics were analyzed. To investigate the effect of miR-BART1-3p overexpression on mRNA expression level of gastric cancer cells and construct the protein interaction network of differential genes and the regulatory network of miR-BART1-3p gene. DIANA-MR micro-T, miRnada, miRDB, TarBase v.8, and ViRBase online databases were used to predict the target genes of miR-BART1-3p and GO enrichment analysis of target gene function was performed. Real-time fluorescence quantitative PCR was used to detect the expression levels of miR-BART1-3p and target genes in SNU719, AGS-OE and AGS gastric cancer cells. The effects of overexpression of EBV-miR-BART1-3p on proliferation, apoptosis, invasion, and migration of gastric cancer cells were investigated by CCK-8, cell cloning, cell scratch and Transwell. [Results] By analyzing the gene expression profile of the GSE51575 dataset, we found that EBVaGC up-regulated the expression of immune cell membrane protein receptors and chemokine family, and was involved in inducing tumor immunity, suggesting a better prognosis. EBVnGC significantly up-regulated the expression of AURK, BUB1B, CCNA2 and CDC20, suggesting the risk of malignant progression and recurrence. High-throughput next-generation sequencing of SNU719 and AGS to detect differences in gene expression revealed that EBVaGC cells (SNU719) up-regulated the expression of genes that inhibit malignant progression as well as potential tumor immunotherapy targets. These results are consistent with those found in the GSE51575 dataset. Fifteen miR-BART1-3p target genes, including FAM168A, TET3, HBP1, ZBTB5, ATXN7L3, KMT5C, SPARC and BMF, were predicted and screened by online tools. After the overexpression of miR-BART1-3p in AGC(EBVnGC) cells, the proliferation, migration, and invasion ability were significantly inhibited, and the signaling pathway promoting tumor progression was also limited in activation. [Conclusions] The overexpression of miR-BART1-3p may inhibit the proliferation and invasion and migration of gastric cancer cells by inhibiting the activation of STAT3/ pSTAT3 and PI3K/AKT signaling pathways and may become a target for the treatment of EBVaGC, which is worthy of further study.
2024-10-01 | GSE241046 | GEO
Project description:mRNA profiling of AGS gastric cancer cell line upon CTNNB1 silencing
| PRJNA261835 | ENA
Project description:Aim: EBV encode at least 44 miRNAs involved in immune regulation and disease progression. Exosomes can be used as carriers of EBV-miRNA-BART intercellular transmission and affect the biological behavior of cells. We characterized exosomes and established a co-culture experiment of exosomes to explore the mechanism of miR-BART1-3p transmission through the exosome pathway and its influence on tumor cell proliferation and invasion. Materials and methods: Exosomes of EBV-positive and EBV-negative gastric cancer cells were characterized by transmission electron microscopy, Nanosight and western blotting, and miRNA expression profiles in exosomes were sequenced with high throughput. Exosomes with high or low expression of miR-BART1-3p were co-cultured with AGS cells to study the effects on proliferation, invasion and migration of gastric cancer cells. The target genes of EBV-miR-BART1-3p were screened and predicted by PITA, miRanda, RNAhybrid, virBase and Diana-Tarbase v.8 databases, and the expression of the target genes after co-culture was detected by qPCR. Results：The exosomes secreted by EBV positive and negative gastric cancer cells range in diameter from 30 nm to 150nm and express the exosomal signature proteins CD63 and CD81. High throughput sequencing showed that exosomes expressed some human miRNAs, among which has-miR-23b-3p, has-miR-320a-3p and has-miR-4521 were highly expressed in AGS-exo. has-miR-21-5p, has-miR-148a-3p and has-miR-7-5p were highly expressed in SNU-719-exo. All EBV miRNAs were expressed in SNU-719 cells and their exosomes, among which EBV- miR-Bart1-5p, EBV- miR-bart22 and EBV- miR-bart16 were the highest in SNU-719 cells. EBV-miR-BART1-5p, EBV-miR-BART10-3p and EBV-miR-BART16 were the highest in SNU-719-exo. After miR-BART1-3p silencing in gastric cancer cells, the proliferation, healing, migration and invasion of tumor cells were significantly improved. Laser confocal microscopy showed that exosomes could carry miRNA into recipient cells. After co-culture with miR-BART1-3p silenced exosomes, the proliferation, healing, migration and invasion of gastric cancer cells were significantly improved. The target gene of miR-BART1-3p was FMA168A, MACC1, CPEB3, ANKRD28 and USP37 after screening by targeted database. CPEB3 was not expressed in all exosome co-cultured cells, while ANKRD28, USP37, MACC1 and FAM168A were all expressed to varying degrees. USP37 and MACC1 are down-regulated after up-regulation of miR-BART1-3p, which may be the key target genes for miR-BART1-3p to regulate the proliferation of gastric cancer cells through exosomes. Conclusions: miR-BART1-3p can affect the growth of tumor cells through exosome pathway. The proliferation, healing, migration and invasion of gastric cancer cells were significantly improved after co-culture with exosomes of miR-BART1-3p silenced expression. USP37 and MACC1 may be potential target genes of miR-BART1-3p in regulating cell proliferation.
2023-03-13 | GSE227017 | GEO
Project description:Gastric cancer is one of the most common cancers worldwide. Epstein-Barr virus-associated gastric cancer accounts for approximately 10% of all gastric cancers. EBV expresses its own proteins and miRNAs (BART miRNAs) and regulates host gene expression. In this study, we examined the effect of EBV infection on host mRNA expression. Differential gene expression was analyzed between EBV-negative human gastric cancer cell line AGS and EBV-positive human gastric cancer cell line AGS-EBV.
2019-10-14 | GSE135644 | GEO
Project description:Cancer cachexia is a multifactorial metabolic syndrome defined by the rapid loss of skeletal muscle mass and the loss of fat mass. Up 80% of cancer patients at the late stage with cachexia suffer from progressive atrophy of adipose tissue. Unlike studies on skeletal muscle wasting, there is limited research on fat loss in cachexia. It was noted that most patients suffer from fat loss as cancer progress. Fat loss precedes muscle loss, is associated with shorter survival, and is variable to timing and intensity in various cancer populations. Increased lipolysis may be the leading cause of fat loss in cancer cachexia. miRNAs are a class of non-coding RNAs of 19~25 nucleotides that regulate gene silencing by interacting with the 3’ untranslated region (UTR) of target mRNA to cause mRNA degradation and translational repression. miRNAs play multifaceted roles in pancreatic cancer proliferation, survival, metastasis, and chemoresistance. Aberrant expression of miRNA in circulating exosomes may play potential roles in modulating fat loss in cancer cachexia. We identified 2 miRNAs, miR-16 and miR-29, which have 2-fold higher expression existed in at PDAC cells. To explore which genes in adipogenesis and lipolysis were directly affected by miR-16-5p or/and miR-29a-3p, we analyzed the targets which were down-regulated in both miR-16-5p and miR-29a-3p-transfected 3T3-L1 cells by mass analysis.
2024-06-13 | PXD037862 | Pride
Project description:Cancer cachexia is a multifactorial metabolic syndrome defined by the rapid loss of skeletal muscle mass and the loss of fat mass. Up 80% of cancer patients at the late stage with cachexia suffer from progressive atrophy of adipose tissue. Unlike studies on skeletal muscle wasting, there is limited research on fat loss in cachexia. It was noted that most patients suffer from fat loss as cancer progress. Fat loss precedes muscle loss, is associated with shorter survival, and is variable to timing and intensity in various cancer populations. Increased lipolysis may be the leading cause of fat loss in cancer cachexia. miRNAs are a class of non-coding RNAs of 19~25 nucleotides that regulate gene silencing by interacting with the 3’ untranslated region (UTR) of target mRNA to cause mRNA degradation and translational repression. miRNAs play multifaceted roles in pancreatic cancer proliferation, survival, metastasis, and chemoresistance. Aberrant expression of miRNA in circulating exosomes may play potential roles in modulating fat loss in cancer cachexia. We identified 2 miRNAs, miR-16 and miR-29, which have 2-fold higher expression existed in at PDAC cells. To explore which genes in adipogenesis and lipolysis were directly affected by miR-16-5p or/and miR-29a-3p, we analyzed the targets which were down-regulated in both miR-16-5p and miR-29a-3p-transfected 3T3-L1 cells by mass analysis.
2024-06-13 | PXD037998 | Pride
Project description:Persistent colonization of the gastric mucosa by Helicobacter pylori (Hp) elicits chronic inflammation and aberrant epithelial cell proliferation, which increases the risk of gastric cancer. We examined the ability of microRNAs to modulate gastric cell proliferation in response to persistent Hp infection and found that epigenetic silencing of miR-210 plays a key role in gastric disease progression. Importantly, DNA methylation of the miR-210 gene was increased in Hp-positive human gastric biopsies as compared to Hp-negative controls. Moreover silencing of miR-210 in gastric epithelial cells promoted proliferation. We identified STMN1 and DIMT1 as miR-210 target genes and demonstrated that inhibition of miR-210 expression augmented cell proliferation by activating STMN1 and DIMT1. Together, our results highlight inflammation-induced epigenetic silencing of miR-210 as a mechanism of induction of chronic gastric diseases, including cancer, during Hp infection. To identify miR-210 targets in gastric cells, whole transcriptome analysis of AGS and MKN45 cells transfected with pre-miR-210 was conducted using Affymetrix GeneChip Human Genome U133 Plus 2.0 Array.
2014-09-04 | E-GEOD-58004 | biostudies-arrayexpress
Project description:Ornithogalum is one of the therapeutic formulation used in homeopathic treatments. It is specifically used in the treatment for gastric and duodenal ulcerations. Towards understanding the anticancer mechanism, we investigated the genome-wide mRNA changes upon treating AGS Gastric Cancer cells with Ornithogalum. We observed that totally 707 genes were significantly regulated upon Ornithogalum Treatment, among them 246 genes were upregulated and 461 genes were downregulated. The results provide insight into molecular implication and gene level expression of AGS upon treatment with Ornithogalum. Total RNA was isolated from AGS gastric cancer cells treated with 0.01% of ornithogalum and ethanol control and profiled using Affymetrix Human Gene 1.0 ST Array (HuGene-1_0-st).
2014-04-01 | E-GEOD-54658 | biostudies-arrayexpress
Project description:We investigate the expression of miRNA in exosome of EBV-positive gastric carcinoma cells. The exosomes of EBV-positive and negative gastric carcinoma cells were separated by ultracentrifugation, the morphology of exosomes was identified by transmission electron microscopy, the exosome size was analyzed by Nanosight, and the expression of exosome membrane protein CD63 and CD81 was detected by western blot. High-throughput sequencing was used to detect miRNA expression profiles in gastric cancer cell lines and their exosomes. Under the ultra-microscopic electron microscope, the exosomes are seen as a typical translucent cup-like structure or a flat spherical structure. The nanoparticle tracking analyzer (Nanosight) showed that the exosomes were between 30 and 150 nm in diameter. Western blot(WB) assays showed that exosomes secreted by EBVaGC and EBVnGC cells expressed specific exosome membrane-associated proteins CD63 and CD81. High-throughput sequencing revealed that EBVaGC(SNU-719) and EBVnGC(AGS) and their secreted exosomes were highly expressed with certain human miRNAs, among which AGS-exo was highly expressed with hsa-miR-23b-3p, hsa-miR-320a-3p, and hsa-miR-4521. SNU-719-exo was highly expressed as hsa-miR-21-5p, hsa-miR-148a-3p and hsa-miR-7-5p. Nearly all EBV-related miRNAs (EBV-miRNA) were expressed in SNU-719 cells and their exosomes, among which EBV-miR-BART1-5p, EBV-miR-BART17-3p and EBV-miR-BART18-5p were the highest in SNU-719 cells, EBV-miR-BART1-5p, EBV-miR-BART18-5p and EBV-miR-BART17-3p were the highest in SNU-719-exo.
2022-03-14 | GSE198354 | GEO