Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS [IRIP-seq]

ABSTRACT: The expression of IGF2BP2 in GCs from PCOS patients was detected using RT-qPCR and western blot. We captured IGF2BP2-interacting transcripts, global transcriptome together with alternative splicing by RNA immunoprecipitation sequencing (RIP-seq) and RNA sequencing (RNA-seq). KGN cells transfected with IGF2BP2 overexpressing plasmids and nuclear factor 1 C-type (NFIC) siRNAs, were applied to CCK-8, EdU and TUNEL assays. IGF2BP2 was highly expressed in GCs from PCOS patients. As a RBP, it preferentially bound to the 3’and 5’UTRs of mRNAs with GGAC motif and a newly found GAAG motif. The overexpression of IGF2BP2 changed the transcriptome profile of KGN cells. IGF2BP2 functioned to regulate alternative splicing events (ASEs) and promote cell proliferation through inhibiting exon skipping events of NFIC. In conclusion, we demonstrated that IGF2BP2 promotes granulosa cell proliferation via regulating alternative splicing of NFIC in PCOS. The findings help to better understand the roles of IGF2BP2 in the pathogenesis of PCOS.

ORGANISM(S): Homo sapiens

PROVIDER: GSE191023 | GEO | 2022/05/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS [RNA-seq]

Project description:The expression of IGF2BP2 in GCs from PCOS patients was detected using RT-qPCR and western blot. We captured IGF2BP2-interacting transcripts, global transcriptome together with alternative splicing by RNA immunoprecipitation sequencing (RIP-seq) and RNA sequencing (RNA-seq). KGN cells transfected with IGF2BP2 overexpressing plasmids and nuclear factor 1 C-type (NFIC) siRNAs, were applied to CCK-8, EdU and TUNEL assays. IGF2BP2 was highly expressed in GCs from PCOS patients. As a RBP, it preferentially bound to the 3’and 5’UTRs of mRNAs with GGAC motif and a newly found GAAG motif. The overexpression of IGF2BP2 changed the transcriptome profile of KGN cells. IGF2BP2 functioned to regulate alternative splicing events (ASEs) and promote cell proliferation through inhibiting exon skipping events of NFIC. In conclusion, we demonstrated that IGF2BP2 promotes granulosa cell proliferation via regulating alternative splicing of NFIC in PCOS. The findings help to better understand the roles of IGF2BP2 in the pathogenesis of PCOS.

2022-05-11 | GSE191022 | GEO

IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS

Project description:IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS

| PRJNA789474 | ENA

IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS [IRIP-seq]

Project description:IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS [IRIP-seq]

| PRJNA789393 | ENA

IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS [RNA-seq]

Project description:IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS [RNA-seq]

| PRJNA789394 | ENA

RNA-Seq of wild type and Nfic-/- mice pancreata

Project description:To assess the role of Nfic in pancreatic development and homeostasis we used constitutive Nfic knockout mice.

2023-05-24 | GSE126907 | GEO

NFIC overexpression perturbs normal haematopoeisis by promoting myeloid differentiaon

Project description:Nuclear factor I-C belongs to a family of CTF binding transcription factor which is known for its role cellular differentiation. In our recent study we identified increased expression of NFIC in. AML samples as compared to normal haematpoitic stem and progenitor cells (HSPCs). We also found that overexpression of NFIC in cord blood derived HSPCs perturbed normal haematopoiesis by increasing monocyte production. Therefore in this analysis we aimed to identify the effect of NFIC overexpression in normal HSPCs at single cell level using single cell RNA (scRNA) sequencing. Cluster analysis based on the cellular and functional identities, identified eight clusters according to their terminal differentiation as monocytes, erythrocytes, dendritic cells (DC), megakaryocytes, neutrophils, megakaryocyte-erythroid progenitor cells, basophil/mast progenitor cells and eosinophils. We found that NFIC overexpressing CD34+ HSPCs had increased percentage of monocytes as compared to control. To understand the molecular basis of this, we focussed our analysis on monocytes to determine changes in mRNA expression following NFIC overexpression. We identified 164 and 88 significantly up-regulated and down-regulated genes, respectively (p<0.05, FDR<0.05) in NFIC overexpressing monocytes as compared to control. Pathway analysis identified enrichment in genes involved in mTOR signalling, cancer cell death and survival, energy metabolism pathways and oxidative phosphorylation. Therefore our scRNA suggested that NFIC play a role in monocytic growth development and its overexpression may lead to monocytic bias in normal haematopoiesis.

2023-01-04 | GSE200456 | GEO

An Nfic-Hedgehog Signaling Cascade Regulates Tooth Root Development

Project description:This study aimed to perform transcriptome profiling of Nfic-/- and corresponding control tooth germ at root initiation stage to identify differentially expressed for key regulators of root development. Coordination between the Hertwig’s Epithelial Root Sheath (HERS) and apical papilla (AP) is crucial for proper root development process. The Hedgehog (Hh) signaling pathway and Nfic are both involved in tooth root development.

2017-08-29 | GSE69054 | GEO

Mitochondrial dynamics in ovarian granulosa cells during follicular growth and in human KGN cells

Project description:In the ovary, proliferation and differentiation of granulosa cells (GCs) drive the growth of follicles. This is, in part, dependent on gonadotropins. Our immunohistochemical studies provided hints of mitochondrial biogenesis and intracellular redistribution in GCs of growing follicles. A cellular model, human KGN cells (granulosa cell tumor cells, derived from growing follicles) was used to study aspects of mitochondrial dynamics. To elevate cAMP and thereby mimic gonadotropin actions, forskolin (FSK) was used, which increased KGN cell size and mitochondrial DNA within 24 h. MitoTracker experiments and ultrastructural 3D reconstruction revealed that FSK treatment induced the formation of elaborate mitochondrial networks. H89, a protein kinase A (PKA) inhibitor, reduced network formation. A proteomic analysis indicated that FSK among others elevated levels of regulators of the cytoskeleton and the steroidogenic enzyme CYP11A1, located in mitochondria, was more than 3-fold increased, implying that cAMP/PKA-associated structural changes go in parallel with the acquisition of steroidogenic competence of mitochondria in KGN cells. In summary, in situ observations showed increases in mitochondria and suggested intracellular trafficking in GCs during follicular growth and indicated that they may partially be under the control of gonadotropins/cAMP. In line with this, elevation of cAMP in KGN profoundly affected mitochondria dynamics in a PKA-dependent manner and implicated cytoskeletal changes.

2022-10-14 | PXD032160 | Pride

Genome-wide occupancy map of NFIC in mouse pancreas

Project description:In order to identify direct NFIC target genes, in the context of pancreatic homeostasis, ChIP-seq was performed using pancreata from 8-10 week-old wild type mice.

2023-05-24 | GSE181098 | GEO

Comprehensive molecular features of polycystic ovary syndrome revealed by transcriptome analysis of oocytes and cumulus cells

Project description:We aimed to elucidate the molecular features and identify causative factors for PCOS through an integrated, transcriptomic analysis of oocytes and cumulus granulosa cells (GCs) from the same patients with PCOS

2020-09-08 | GSE155489 | 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