Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Tumor suppressive function of IGF2BP1 in gastric cancer through decreasing MYC

ABSTRACT: Tumor suppressive function of IGF2BP1 in gastric cancer through decreasing MYC

PROVIDER: PRJNA1019241 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26117322_1.fastq.gz	Fastqsanger.gz
	SRR26117322_2.fastq.gz	Fastqsanger.gz
	SRR26117323_1.fastq.gz	Fastqsanger.gz
	SRR26117323_2.fastq.gz	Fastqsanger.gz
	SRR26117324_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Tumor suppressive function of IGF2BP1 in gastric cancer through decreasing MYC

Project description:Gastric cancer is one of the most common causes of cancer-related death worldwide. The N6-methyladenosine (m6A) reader IGF2BP1 (insulin-like growth factor-2 mRNA binding protein 1) has been reported to promote cancer progression by stabilizing oncogenic mRNAs through its m6A-binding activity in some tumors. However, the role of IGF2BP1 in gastric carcinogenesis remains unclear. In this study, we find that IGF2BP1 is significantly downregulated in tumor tissues from patients with gastric cancer. Lower expression of IGF2BP1 is associated with poor prognosis. IGF2BP1 suppresses gastric cancer cell proliferation in an m6A-dependent manner. Additionally, IGF2BP1 is able to significantly attenuate tumor growth of gastric cancer cells. Further m6A sequencing and m6A-RIP (RNA immunoprecipitation) assays show that MYC (c-myc proto-oncogene) mRNA is a target transcript of IGF2BP1 in gastric cancer cells. IGF2BP1 inhibits gastric cancer cell proliferation by reducing the mRNA and protein expression of MYC. Mechanistically, IGF2BP1 promotes the degradation of MYC mRNA and inhibits its translation efficiency. Taken together, these data suggest that IGF2BP1 plays a tumor-suppressive role in gastric carcinogenesis by downregulating MYC in an m6A-dependent manner, thereby making the IGF2BP1-MYC axis a potential target for gastric cancer treatment.

2024-02-26 | GSE243617 | GEO

m6A modification profile in primary microglia with/without Igf2bp1 knockdown

Project description:Our study demonstrated that the expression of Igf2bp1 in activated microglia was significantly up-regulated, implying a role of Igf2bp1 in LPS-induced m6A modifications in microglia. To understand the roles of Igf2bp1 on LPS-induced m6A modification in microglia, we performed Igf2bp1 loss-of-function (LOF) approach. Microglia stimulated by LPS were transfected with either scrambled siRNA control or Igf2bp1 siRNA for 48 hours. To m6A modification profiles in control and Igf2bp1 LOF microglia were determined by MeRIP-seq analysis.

2022-12-31 | E-MTAB-11411 | biostudies-arrayexpress

Helicobacter pylori-mediated Epigenetic Dysregulation of FOXD3 Tumor-suppressive Cascade In Gastric Carcinogenesis [ChIP]

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

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

Helicobacter pylori-mediated Epigenetic Dysregulation of FOXD3 Tumor-suppressive Cascade In Gastric Carcinogenesis [ChIP]

2012-12-28 | GSE39490 | GEO

NINJ2 inhibition increased chemo-sensitivity by decreasing CICs in chemotherapy-resistant gastric cancer

Project description:NINJ2 inhibition increased chemo-sensitivity by decreasing CICs in chemotherapy-resistant gastric cancer

| PRJNA718254 | ENA

Detection of IGF2BP1 phosphorylation in vitro and in vivo via Pro-Alanase treatment

Project description:In this project we aim to identify phosphorylation sites of IGF2BP1 that have not been discovered yet in mass spec experiments due to insufficient coverage. To this end we used Pro-Alanase treatment that produced detectable peptides in regions that are not covered by commonly used approaches. IGF2BP1 phosphorylation was investigated in vitro by treating purified IGF2BP1 with Src and in vivo by comparing immunoprecipitated IGF2BP1 from unstressed and stressed (1.5 h thapsigargin or 2 h or arsenite) HEK293T cells expressing GFP-labeled IGF2BP1.

2024-11-13 | PXD056497 | Pride

NINJ2 inhibition increased chemo-sensitivity by decreasing CICs in chemotherapy-resistant gastric cancer

Project description:One of the first-line chemotherapy regimes for gastric cancer is a combination treatment of epirubicin, cisplatin, and 5-fluorouracil (ECF). Chemoresistance remains the major obstacle to achieving successful results from gastric cancer treatment. Understanding acquired or pre-existing resistance to anticancer drugs is essential to the development of a therapeutic modality for gastric cancer. In this study, we established ECF-resistant (ECF-R) gastric cancer cell lines. We found that nerve injury–induced protein 2 (Ninjurin2, NINJ2) functioned as a biomarker for ECF-R in both gastric cancer cells. We also investigated the NINJ2 binding molecule and downstream pathway using both LC-MS/MS and phospho-antibody arrays.

2024-03-29 | GSE171054 | GEO

YAP/TAZ initiates gastric tumorigenesis via upregulation of MYC

Project description:YAP/TAZ initiates gastric tumorigenesis via upregulation of MYC

| PRJNA413934 | ENA

IGF2BP1 promotes SRF-dependent transcription in cancer in a m6A- and miRNA-dependent manner [IGF2BP1 and SRF KD in ES-2 (total RNA)]

Project description:The oncofetal mRNA-binding protein IGF2BP1 and the transcriptional regulator SRF modulate gene expression in cancer. In cancer cells, we demonstrate that IGF2BP1 promotes the expression of SRF in a conserved and N6-methyladenosine (m6A) dependent manner by impairing the miRNA-directed decay of the SRF mRNA. This results in enhanced SRF-dependent transcriptional activity and promotes tumor cell growth and invasion. At the post-transcriptional level, IGF2BP1 sustains the expression of various SRF-target genes. The majority of these SRF/IGF2BP1-enhanced genes, including PDLIM7 and FOXK1, shows conserved upregulation with SRF and IGF2BP1 synthesis in cancer. PDLIM7 and FOXK1 promote tumor cell growth and were reported to enhance cell invasion. Consistently, 35 SRF/IGF2BP1-dependent genes showing conserved association with SRF and IGF2BP1 expression indicate a poor overall survival probability in ovarian, liver and lung cancer. In conclusion, these findings identify the SRF/IGF2BP1-, miRNome- and m6A-dependent control of gene expression as a conserved oncogenic driver network in cancer.

2018-10-10 | GSE116059 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data