Ontology highlight
ABSTRACT:
PROVIDER: PRJNA349261 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4434640_1.fastq.gz | Fastqsanger.gz | |||
| SRR4434640_2.fastq.gz | Fastqsanger.gz | |||
| SRR4434641_1.fastq.gz | Fastqsanger.gz | |||
| SRR4434641_2.fastq.gz | Fastqsanger.gz | |||
| SRR4434642_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
Similar Datasets
Project description:Analysis of HER2-amplified NCI-N87 gastric cancer cell line exposed to 0.1 µg/mL T-DM1 and subsequently cultured in the presence of gradually increasing doses, up to a maximum of 4 µg/mL. The resultant cell lines that grew exponentially in the presence of T-DM1 were designated as drug resistant gastric cancer cell lines, and named N87-TDMR. We used microarrays to detail the gene expression in N87-TDMR and N87-parent cells to screen for transcripts correlated with T-DM1 resistance.
2017-10-01 | GSE95414 | GEO
Project description:We compared gene expression profiles in trastuzumab-sensitive NCI-N87 cell line versus four trastuzumab-resistant cell lines (N87-TR1, N87-TR2, N87-TR3, N87-TR4) by microarray analysis in order to identify groups of genes associated with a specific signaling pathway or biological process.
2017-02-13 | GSE77346 | GEO
Project description:ATAC-seq of human gastric adenocarcinoma NCI-N87 cell line treated with lapatinib
| PRJEB44102 | ENA
Project description:Background: Egl-9 family hypoxia inducible factor 3 (EGLN3) belongs to the family of 2-oxoglutarate (2-OG)- and ferrous iron (Fe 2+)-dependent dioxygenases, which play critical roles in all steps of tumorigenesis. Previous studies have found that EGLN3 regulates the malignant biological behavior of malignant tumors. However, its role and mechanism in the occurrence and development of gastric cancer (GC) are still unclear. This study aimed to investigate the role of EGLN3 in gastric carcinogenesis Methods:Bioinformatics analysis, qRT-PCR, western blot, CCK-8, and in vivo xenograft tumor model were used to examine the expression and function of EGLN3. Survival analysis was performed to determine the correlation between EGLN3 expression and prognosis of patients with GC. Genes modulated by EGLN3 in NCI-N87 cells were identified through RNA next generation sequence screening and further verified by qRT-PCR in NCI-N87 cells. Results: EGLN3 expression was markedly reduced in GC tissues as compared with that in normal tissues. Likewise, EGLN3 expression was also significantly reduced in a panel of GC cell lines . Forced expression of EGLN3 inhibited proliferation in NCI-N87 cells in vitro. Additionally, EGLN3 impaired growth of NCI-N87 cells in immunodeficient mice. Survival analysis showed that EGLN3 expression was positively associated with favorable outcome in patients with GC.
2024-04-12 | GSE200646 | GEO
Project description:MicroRNAs (miRNAs) play an important role in the regulation of gene expression and are often dysregulated in disease. The recent development of the CRISPR-Cas9 gene-editing system, composed of the Cas9 nuclease in complex with a single guide RNA (sgRNA), allows researchers to direct DNA cleavage at a predetermined site and to conduct genome-scale knockout screens. To determine the functional role of miRNAs in cancer, we designed and constructed a library of 7,382 sgRNAs to target 85% of the 1,881 annotated human miRNA stem-loops. We then examined the role of miRNAs in HeLa cell fitness by monitoring the change in frequency of each sgRNA over time. We identified 44 pro-proliferative miRNAs from two replicate experiments, including miR-31, a known cervical cancer overexpressing miRNA that enhances HeLa cell proliferation. We also examined the role of miRNAs in NCI-N87 gastric cancer cells and identified 10 pro-fitness and 10 anti-fitness miRNAs. In both screens, many of the pro-fitness miRNAs identified are overexpressed in tumors cervical tumors for HeLa or gastric tumors for NCI-N87. In summary, we present a CRISPR miRNA-targeted screen which was able to identify both known and novel fitness-associated miRNAs in the HeLa and NCI-N87 cell lines.
2018-06-21 | GSE110784 | GEO
Project description:Background: Zinc finger and scan domain containing 18 (ZSCAN18) belongs to zinc finger transcription factor superfamily, which consists of the hundreds of members that play critical roles in all steps of tumorigenesis. Although hypermethylation of ZSCAN18 promoter and its consequent deficiency in a variety of malignancies has been reported recently, its functions and mechanisms in the initiation and progression of gastric cancer (GC) are not clear. This study aims to investigate the roles of ZSCAN18 in gastric carcinogenesis. Methods: Methylation of ZSCAN18 promoter in GC cell lines were analyzed via MassARRAY and treatment of 5-Aza-2'-deoxycytidine. Bioinformatics analysis, qRT-PCR, western blot, immunohistochemistry, CCK-8, colony formation, and in vivo xenograft tumor model were used to examine the expression and function of ZSCAN18. Survival analysis was performed to determine the correlation between ZSCAN18 expression and prognosis of patients with GC. Genes modulated by ZSCAN18 in NCI-N87 cells were identified through RNA next generation sequence screening and further verified by qRT-PCR in AGS and NCI-N87 cells. Results: ZSCAN18 expression was markedly reduced in GC tissues as compared with that in adjacent normal tissues due to hypermethylation in GC. Likewise, ZSCAN18 expression was also significantly reduced in a panel of GC cell lines as the result of densely methylated ZSCAN18 promoter. Forced expression of ZSCAN18 inhibited proliferation in AGS and NCI-N87 cells in vitro. Additionally, ZSCAN18 impaired growth of NCI-N87 cells in immunodeficient mice. Survival analysis showed that ZSCAN18 expression was positively associated with favorable outcome in patients with GC. RNA next generation sequence screening showed three representative genes (FGF20, CEACAM5 and TP53INP2) involved in downstream signaling pathways modulated by ZSCAN18. Conclusions: Collectively, this study unveils the anti-cancer role of ZSCAN18 in GC, providing a promising diagnostic and therapeutic target.
2024-10-13 | GSE186232 | GEO
Project description:Glycomic analysis of total N-glycan species released from ErbB2 isolated from WT and ST6GAL1 K.O. ErbB2-positive gastric cancer cells (NCI-N87)
2020-02-11 | MSV000084943 | MassIVE
Project description:Forkhead box (Fox) proteins constitute an evolutionarily conserved family of transcriptional regulators whose deregulations lead to tumorigenesis. However, their regulation and function in gastric cancer are unknown. Promoter hypermethylation occurs during Helicobacter pylori (H pylori)-induced gastritis, but whether the deregulated genes contribute to the multi-step gastric carcinogenesis remains unclear. FOXD3 was found to be hypermethylated in a mouse model of H pylori infection and possess tumor-suppressive functions in gastric cancer cell lines. In order to characterize the direct targets of FOXD3 that confer its actions, we performed ChIP-chip in N87 gastric cancer cell line which express low level of FOXD3 in the nuclei of a sub-population of cells. Promoter hypermethylation occurs during Helicobacter pylori (H pylori)-induced gastritis, but whether the deregulated genes contribute to the multi-step gastric carcinogenesis remains unclear. We used MethylCap-microarray to identify hypermethylated genes in a mouse model of H pylori infection. human Samples: Human gastric tumor cell line, N87 was grown in RPMI1640 supplemented with 10% fetal bovine serum. ChIP assays were performed using anti-FOXD3 antibody. The immunoprecipitated-FOXD3 and -IgG DNA were used to probe the Agilent human ChIP-chip arrays. mouse Samples: Two-condition experiment, H pylori-infected vs. control gastric tissues. 2 dye-swap replicates.
2012-12-28 | E-GEOD-39490 | biostudies-arrayexpress
Project description:Purpose: To understand how SCAMP1 drives the proliferation of GC cells, endogenous SCAMP1 expression was reduced using shRNA in gastric cancer cell line NCI-N87. RNA sequencing was performed to characterize differentially expressed genes (DEGs) betwenn the control (shCtrl) and the SCAMP1-depleted (shS1#1) NCI-N87 cells. Methods: When shCtrl and shS1#1 NCI-N87 cells grew to approximately 80% confluence, these cells were washed twice using pre-chilled PBS. Total RNAs were extracted using Trizol reagents (Thermo Fisher Scientific). Poly(A) mRNAs were isolated and enriched using NEBNext Poly(A) mRNA Magnetic Isolation Module. Library was generated with NEBNext ® Ultra™ Directional RNA Library Prep Kit for Illumina (NEB, E7420S) following the manufacturer’s instruction, and library was then sequenced by Novogene (Beijing, China). FastQC was used to examine the quality of raw reads. Read alignment was conducted using STAR (v2.5.1b), and R package edgeR (v3.8.5) was used to determine relative transcript abundance and differentially expressed genes (DEGs) between shCtrl and shS1#1 sample. Results: Generally, the expressions of 495 genes increased whereas the expressions of 204 genes decreased in shS1#1 cells, compared with shCtrl cells (|log2FC| > 1 and P < 0.05). Gene Ontology (GO) analysis indicated that significant portion of these differentially expressed genes were enriched in ligand-receptor interactions, such as fibroblast growth factor receptor binding, and the downstream signaling pathways, such as PI3K-Akt pathway. Conclusions: Reduced SCAMP1 expression attenuates the proliferation in GC cells via deactivating multiple pro-tumoral signaling pathways.
2024-09-25 | GSE252526 | GEO
Project description:The human adrenocortical carcinoma cell line NCI-H295R treated with siRNA targeting SF-1 or RNF31 with luciferase-targeting siRNA as control. Combined with forskolin treatment.
2012-02-01 | E-MEXP-3259 | biostudies-arrayexpress