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Role of FGF-2 induced non-coding RNA in cancer [I]

ABSTRACT: We show that IER3 and IER3-AS1 protein coding and non-coding genes mediates oncogenic properties in cancer cell lines when they are induced by FGF-2 which is fibroblast growth factor. Comprehensive analysis of mechanisms behind the regulation of these genes by FGF-2 induction is shown in this study.

ORGANISM(S): Homo sapiens

PROVIDER: GSE189962 | GEO | 2022/06/24

REPOSITORIES: GEO

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Role of FGF-2 induced non-coding RNA in cancer [II]

Project description:We show that IER3 and IER3-AS1 protein coding and non-coding genes mediates oncogenic properties in cancer cell lines when they are induced by FGF-2 which is fibroblast growth factor. Comprehensive analysis of mechanisms behind the regulation of these genes by FGF-2 induction is shown in this study.

2022-06-24 | GSE190211 | GEO

Role of hnRNPK in FGF-2 induced non-coding RNA in cancer

Project description:We show that IER3 and IER3-AS1 protein coding and non-coding genes mediates oncogenic properties in cancer cell lines when they are induced by FGF-2 which is fibroblast growth factor. Mechanistic studies show that these two RNAs are regulated by hnRNPK. Hence, we investigated the role of hnRNPK by knocking down this gene and studying the changes in the global targets including IER3 and IER3-AS1.

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IER3-AS1 interacting proteins by AP-MS

Project description:Characterisation IER3-AS1 interacting proteins using chromatin oligo-affinity precipitation (ChOP) followed by mass spectrometry. The HeLa cell lysates was incubated with biotinylated antisense oligonucleotides (ASO), targeting an experimental target antisense long noncoding RNA IER3-AS1 or a control RNA LacZ. LacZ and IER3-AS1 interacting proteomes were pulldown using Streptavidin beads. The eluted protein samples from both LacZ control ASOs and IER3-AS1 ASOs subjected to mass-spectrometry analyses to identify IER3-AS1 interacting proteins.

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FGF Receptor and Wnt-1 Signaling Cooperate in Mammary Tumorigenesis

Project description:The fibroblast growth factor pathway is known to cooperate with the highly oncogenic Wnt/ï¢-catenin pathway in mouse models of breast cancer. To investigate the mechanisms involved in this cooperativity, we utilized MMTV-driven transgenic mouse lines expressing a drug-inducible model for FGF Receptor signaling (iFGFR) crossed with the previously characterized MMTV-Wnt-1 mouse model. In these bigenic mice, both iFGFR1 and iFGFR2 activation resulted in a dramatic enhancement of mammary tumorigenesis. Tumor microarray analysis identified no transcriptional enhancement of Wnt/ï¢-catenin targets, however, identified a protein translational gene signature that also correlated with elevated FGFR1 and FGFR2 expression in several human breast cancer data sets. Additionally, iFGFR1 activation resulted in enhanced polysome recruitment and a marked increase in protein expression of several different Wnt/ï¢-catenin target oncogenes. Rapid FGFR-induced ERK activation and phosphorylation of key translation regulators was observed both in vivo in the transgenic mouse model, and in human breast cancer cell lines treated with exogenous FGF. These studies suggest that translational regulation is a key rate-limiting step required for oncogenic cooperativity between the Wnt and FGF pathways. reference X sample

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Transcription profiling of Xenopus embryos in which fibroblast growth factor (FGF) signalling was inhibited by two different dominant negative FGF receptors

Project description:Genes regulated by the fibroblast growth factor (FGF) signalling pathway were indentified in the early development of the amphibian Xenopus laevis by comparing gene expression in control embryos and embryos in which FGF signalling was inhibited by two different dominant negative FGF receptors.

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Role of FGF-2 induced non-coding RNA in cancer

Project description:Role of FGF-2 induced non-coding RNA in cancer

| PRJNA786344 | ENA

FGF Receptor and Wnt-1 Signaling Cooperate in Mammary Tumorigenesis

Project description:The fibroblast growth factor pathway is known to cooperate with the highly oncogenic Wnt/beta-catenin pathway in mouse models of breast cancer. To investigate the mechanisms involved in this cooperativity, we utilized MMTV-driven transgenic mouse lines expressing a drug-inducible model for FGF Receptor signaling (iFGFR) crossed with the previously characterized MMTV-Wnt-1 mouse model. In these bigenic mice, both iFGFR1 and iFGFR2 activation resulted in a dramatic enhancement of mammary tumorigenesis. Tumor microarray analysis identified no transcriptional enhancement of Wnt/beta-catenin targets, however, identified a protein translational gene signature that also correlated with elevated FGFR1 and FGFR2 expression in several human breast cancer data sets. Additionally, iFGFR1 activation resulted in enhanced polysome recruitment and a marked increase in protein expression of several different Wnt/beta-catenin target oncogenes. Rapid FGFR-induced ERK activation and phosphorylation of key translation regulators was observed both in vivo in the transgenic mouse model, and in human breast cancer cell lines treated with exogenous FGF. These studies suggest that translational regulation is a key rate-limiting step required for oncogenic cooperativity between the Wnt and FGF pathways.

2010-03-01 | GSE17916 | GEO

Role of FGF-2 induced non-coding RNA in cancer [I]

Project description:Role of FGF-2 induced non-coding RNA in cancer [I]

| PRJNA785255 | ENA

Role of FGF-2 induced non-coding RNA in cancer [II]

Project description:Role of FGF-2 induced non-coding RNA in cancer [II]

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An FGF-2 signaling pathway that is activated in aged skeletal muscle promotes intramuscular adipogenesis

Project description:Aged skeletal muscle is markedly affected by fatty muscle infiltration and strategies to reduce the occurrence of adipocytes within skeletal muscle, the intramuscular adipose tissue (IMAT), are urgently needed. Fibroblast growth factor-2 (FGF-2) is a critical growth factor for muscle tissue. Here, we show that FGF-2 not only stimulates muscle growth, but also promotes intramuscular adipogenesis. Using multiple screening assays for upstream and downstream signaling of microRNA (miR)-29a we located the secreted protein and adipogenic inhibitor SPARC to an FGF-2 signaling pathway that is conserved between skeletal muscle cells from mice and humans and that is activated in skeletal muscle from aged mice. FGF-2 induces the miR-29a/SPARC axis through transcriptional activation of FRA-1 which binds and activates an evolutionary conserved AP-1 site element proximal in the miR-29a promoter. Genetic deletions in muscle cells and AAV-mediated overexpression of FGF-2 or SPARC in mouse skeletal muscle revealed that this axis regulates differentiation of fibro/adipogenic progenitors in vitro and intramuscular fat formation in vivo. Thus, our data highlight an ambivalent role of FGF-2 for adult skeletal muscle and reveal a novel pathway to combat fat accumulation in aged skeletal muscle.

2021-08-23 | PXD020575 | Pride

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