Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression profiling of cervical cancer cells with IGF2R knock down

ABSTRACT: From comprehensive expression analysis of RNAseq data, IGF2R was found to correlate with poor prognosis in cervical cancer. Gene knockdown of IGF2R lead to cell death in cervical cancer. To reveal its biological function, we performed microarray analysis using IGF2R knockdown cervical cancer cells. We used microarrays to detail the gene expression alteration by IGF2R gene knockdown by siRNA transfection.

ORGANISM(S): Homo sapiens

PROVIDER: GSE137998 | GEO | 2019/11/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression profiling of cervical cancer cells with IGF2R knock down

Project description:Expression profiling of cervical cancer cells with IGF2R knock down

| PRJNA574126 | ENA

Knock down of FTO in cervical cancer cells

Project description:FTO, an N6-methyladenosine (m6A) demethylase, can promote cervical cancer cell proliferation and migration. RNA-sequencing of SiHa cells with FTO knockdown was conducted to dissect the differentially expressed genes and the potential mechanism of FTO in cervical cancer.

2020-02-13 | GSE133517 | GEO

Knock down of FTO in cervical cancer cells

Project description:Knock down of FTO in cervical cancer cells

| PRJNA551671 | ENA

Airn transcriptional overlap but not its lncRNA products induce imprinted Igf2r silencing.

Project description:To test if the imprinted long non-coding RNA (lncRNA) Airn transcription or its product silences the protein-coding Igf2r gene, we shortened the endogenous lncRNA to four different lengths by inserting polyadenylation (polyA) cassettes on the paternal chromosome via homologous recombination in ES cells. ES cell differentiation was used to recapitulate the developmental onset of Airn and Igf2r imprinted expression and polyA cassettes inserted before (T3, T16, T27) or after (T31, T51) the Igf2r promoter successfully truncated Airn, with the exception of T27. RNA hybridization to a tiling array (MIRTA) demonstrated loss of Airn upstream of the Igf2r promoter (except T27) and absence of novel spliced variants in all truncation alleles. To further test the transcriptional overlap model we moved the Airn promoter ~700bp before the Igf2r TSS in ES cells that lack an endogenous paternal Airn promoter and called this cell line FAP (Forward-Airn-Promoter). RNA hybridization to a tiling array (MIRTA) demonstrated that the moved Airn promoter expresses Airn in wildtype orientation and terminates at the wildtype 3' end. ES cell lines expressing different Airn variants were differentiated on gelatinized dishes after feeder cell depletion and LIF withdrawal by 0.27M-BM-5M retinoic acid for 5 days and Airn length was assayed.

2012-12-20 | E-GEOD-41444 | biostudies-arrayexpress

Cervical cancer

Project description:Cervical cancer

| PRJNA144107 | ENA

GNPS Comparable plasma lipid changes in patients with high-grade cervical intraepithelial neoplasia and patients with cervical cancer

Project description:Comparable plasma lipid changes in patients with high-grade cervical intraepithelial neoplasia and patients with cervical cancer

2020-10-22 | MSV000086351 | GNPS

Airn transcriptional overlap but not its lncRNA products induce imprinted Igf2r silencing.

2012-12-20 | GSE41444 | GEO

IGF2R-initiated Proton Rechanneling Dictates an Anti-inflammatory Property in Macrophages

Project description:Metabolic trait in macrophages can be rewired by insulin like growth factor 2 (IGF2), however, how IGF2 modulates the cellular dynamics and functionality remains unclear. We demonstrate here that IGF2 exhibits dual and opposing roles in controlling inflammatory phenotypes in macrophages via regulating glucose metabolism. Such difference relies on the dominant activation of IGF2R by low dose IGF2 and IGF1R by high dose IGF2. IGF2R activation leads to proton rechanneling to the mitochondrial intermembrane space, and enables sustained oxidative phosphorylation. Mechanistically,low dose IGF2 induces nucleus translocation of IGF2R that promotes Dnmt3a-mediated DNA methylation via activating GSK3β, and subsequently impairs the expression ofvacuolar-type H+-ATPase (v-ATPase).This sequestrated assembly of v-ATPase inhibits the channeling of protons to lysosomes and leads to their rechanneling to mitochondria. An IGF2R-specific IGF2 mutant only induces anti-inflammatory response and inhibits colitis progression. Altogether, our findings highlight a novel role of IGF2R activation in dictating anti-inflammatory macrophages.

2020-12-07 | GSE151404 | GEO

Knock down of APE1 suppressed gastric cancer metastasis via improving immune disorders caused by myeloid-derived suppressor cells

Project description:Gastric cancer is a highly immunogenic malignancy. Immune tolerance facilitated by myeloid-derived suppressor cells (MDSCs) has been implicated in gastric cancer resistance mechanisms. The potential role of APE1 in regulating gastric cancer metastasis by targeting MDSCs remains uncertain. In this study, the plasmid Plxpsp-mGM-CSF was used to induce high expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) in GES-1 cells. For tumor transplantation experiments, AGS, AGS+GM-CSF and AGS+GM-CSF-siAPE1 cell lines were established by transfection, followed by subcutaneous implantation of tumor cells. MDSCs, Treg cells, IgG, CD3 and CD8 levels were assessed. Transfection with siAPE1 significantly inhibited tumor growth compared to the AGS+GM-CSF group. APE1 gene knockdown modulated the immune system in gastric cancer mice, characterized by a decrease in MDSCs and an increase in Treg cells, IgG, CD3 and CD8. In addition, APE1 gene knockdown resulted in decreased levels of pro-MDSC cytokines (HGF, CCL5, IL-6, CCL12). Furthermore, APE1 gene knockdown inhibited proliferation, migration and invasion of AGS and MKN45 cells. AGS-GM-CSF cell transplantation increased MDSC levels and accelerated tumor growth, whereas APE1 knockdown reduced MDSC levels, inhibited tumor growth and attenuated inflammatory infiltration in gastric cancer tissues.

2024-06-05 | GSE262050 | GEO

Role of IGF2R in beta cells

Project description:Role of IGF2R in beta cells

| PRJNA1061312 | ENA