Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Undefined

ABSTRACT: Bulk 3-prime RNAsequencing of MYC-overexpressing gastric cancer cell lines derived from mouse gastric neuroendocrine carcinomas

PROVIDER: PRJEB61969 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR11422937_1.fastq.gz	Fastqsanger.gz
	ERR11422937_2.fastq.gz	Fastqsanger.gz
	ERR11422938_1.fastq.gz	Fastqsanger.gz
	ERR11422938_2.fastq.gz	Fastqsanger.gz
	ERR11422939_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 72

Similar Datasets

undefined

Project description:Bulk 3-prime RNA-sequencing of macrodissected neuroendocrine and exocrine tumor components of FFPE-embedded mouse gastric neuroendocrine carcinomas

| PRJEB61968 | ENA

undefined

Project description:Whole exome sequencing data of mouse cancer cell lines derived from mouse gastric neuroendocrine carcinomas

| PRJEB61970 | ENA

undefined

Project description:Low coverage whole genome sequencing of mouse cancer cell lines derived from mouse gastric neuroendocrine carcinomas

| PRJEB61972 | ENA

undefined

Project description:Genome-wide CRISPR/Cas9 LOF screen data performed in mouse cancer cell lines derived from mouse gastric neuroendocrine carcinomas

| PRJEB61971 | ENA

Stomach-specific c-Myc overexpression drives intestinal-type gastric cancer in mice via AKT/mTOR signaling

Project description:Gastric cancer (GC) is one of the most common malignant cancers in the world. c-Myc, a well-known oncogene, is commonly amplified in many cancers, including gastric cancer. However, it is still not completely understood how c-Myc functions in GC. Here, we generated a stomach-specific c-Myc knock-in mouse model to investigate its role in GC. We found that overexpression of c-Myc in Atp4b+ gastric parietal cells could induce intestinal-type gastric cancer in mice. Mechanistically, c-Myc promoted tumorigenesis via the AKT/mTOR pathway. Furthermore, AKT inhibitor (MK-2206) or mTOR inhibitor (Rapamycin) inhibited the proliferation of c-Myc overexpressing gastric cancer cell lines. Thus, our findings highlight that gastric cancer can be induced by c-Myc overexpression through activation of the AKT/mTOR pathway.

2021-08-11 | GSE145583 | GEO

SLE and atherosclerosis CD4+ T-cell RNAsequencing

Project description:Bulk RNAsequencing of CD4+ T-cells in SLE patients with (SLE-P) and without (SLE-NP) subclinical atherosclerotic plaques in carotid and femoral arteries, scanned by vascular ultrasound.

2024-10-10 | E-MTAB-13443 | biostudies-arrayexpress

SLE and atherosclerosis CD8+ T-cell RNAsequencing

Project description:Bulk RNAsequencing of CD8+ T-cells in SLE patients with (SLE-P) and without (SLE-NP) subclinical atherosclerotic plaques in carotid and femoral arteries, scanned by vascular ultrasound.

2024-10-10 | E-MTAB-13444 | biostudies-arrayexpress

Label-free whole cell proteomics for oncogene cell lines

Project description:Label-free whole cell proteomics was performed for the following cell lines: LHS-PREC engineered to overexpress MYC or EV; P4936 overexpressing MYC on a tetracycline-repressible promotor; MCF10A cells expressing signal transduction oncogenes AKT, BRAF, EGFR, HER2, KRAS, MEK; KP4 and PSN1 PDAC cell lines vs HPDE normal pancreatic cell; PDX-derived osteosarcoma cell lines with MYC amplification vs hFOB cell

2022-08-11 | PXD033373 | Pride

Transcription profiling by array of 5-Aza-2’-deoxycytidine treated gastric cancer cell lines

Project description:DNA methylation is a key contributor to normal mammalian development, although, abnormal CpG islands methylation has been described to have a role in carcinogenesis. In gastric cancer, it is observed a global hypomethylation within the bulk genome and local hypermethylation at specific tumor suppressor genes. Conversely, the absence of DNA methylation may be an important step in stable transcriptional activation of oncogenes, contributing to tumor development. The screening of genes modulated by DNA methylation in gastric cancer may contribute to the identification of tumor suppressor genes and/or oncogenes modulated by DNA methylation never described in this neoplasia. In this experiment we aimed to identify differentially expressed genes by comparing 5-Aza-2’-deoxycytidine (5-AZAdC)-treated and non-treated gastric cancer cell lines. 5-AZAdC is a demethylation agent and has received FDA approval for the treatment of myelodysplastic syndromes. This drug has also showed capacity to treat solid tumors with low dose. The ACP02 and ACP03 gastric cancer cell lines used in this experiment were previously established by our research group from primary gastric adenocarcinomas classified as diffuse and intestinal types, respectively. Both cell lines present chromosome 8 trisomy, MYC amplification, and TP53 loss of copy. Moreover, ACP03 is able to start a tumorigenesis process in Cebus apellas.

2019-04-30 | E-MTAB-7880 | biostudies-arrayexpress

Gene expressions of human gastric cancer cell lines

Project description:We compared gene expressions between two gastric cancer cell lines overexpressing RHOA wild-type or Y42C

2023-06-08 | GSE152041 | GEO