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YTHDF2 inhibits gastric cancer cell growth by regulating FOXC2 signaling pathway

ABSTRACT: We found that YTHDF2 has lower expression in GC tissues and GC cells, and promotes the growth, migration and invasion of GC cells. In addition, the analysis of clinical data found that the expression level of YTHDF2 was closely related to the stage of GC and the survival of patients with GC. RNA-seq showed that overexpression of YTHDF2 significantly reduced protein expression in the FOXC2 (Forkhead box protein C2, FOXC2) signaling pathway.

ORGANISM(S): Homo sapiens

PROVIDER: GSE162004 | GEO | 2021/01/28

REPOSITORIES: GEO

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YTHDF2 inhibits gastric cancer cell growth by regulating FOXC2 signaling pathway

Project description:we found that YTHDF2 has lower expression in GC tissues and GC cells, and promotes the growth, migration and invasion of GC cells. In addition, the analysis of clinical data found that the expression level of YTHDF2 was closely related to the stage of GC and the survival of patients with GC. RNA-seq showed that overexpression of YTHDF2 significantly reduced protein expression in the FOXC2 (Forkhead box protein C2, FOXC2) signaling pathway.

2021-05-05 | GSE168611 | GEO

YTHDF2 inhibits gastric cancer cell growth by regulating FOXC2 signaling pathway

Project description:YTHDF2 inhibits gastric cancer cell growth by regulating FOXC2 signaling pathway

| PRJNA680305 | ENA

YTHDF2 inhibits gastric cancer cell growth by regulating FOXC2 signaling pathway

Project description:YTHDF2 inhibits gastric cancer cell growth by regulating FOXC2 signaling pathway

| PRJNA713007 | ENA

YTHDF2 Inhibits Gastric Cancer Cell Growth by Regulating FOXC2 Signaling Pathway.

Project description:BackgroundGastric cancer (GC) is one of the most common malignancies in the world, and the fourth most frequent malignancy worldwide. YTHDF2 (YTH domain family 2, YTHDF2) binds to mRNA containing m6A, thereby regulating the localization and stability of the bound mRNA. YTHDF2 was shown to be associated with some cancer patient prognosis. However, the effect of YTHDF2 on gastric cancer and the molecular mechanism of this effect have not been documented.MethodsTo conduct this research, YTHDF2 expression levels in public databases and gastric cancer patient samples were analyzed. The effects of YTHDF2 on the growth of gastric cancer cells were detected in vivo and in vitro. RNA-seq was used to analyze the signal pathways regulated by YTHDF2, and experiments were carried out for verification.ResultsIn our study, we found that YTHDF2 has lower expression in GC tissues and GC cells, and inhibits the growth of GC cells. In addition, the analysis of clinical data found that the expression level of YTHDF2 is closely related to the stage of GC and the survival of patients with GC. RNA sequencing results showed that overexpression of YTHDF2 significantly reduced protein expression in the FOXC2 (Forkhead box protein C2, FOXC2) signaling pathway. Finally, we found that knockout of FOXC2 reversed the inhibitory effect of YTHDF2 on GC cells.ConclusionIn summary, YTHDF2 inhibits the growth of GC cells by negatively regulating FOXC2 and may serve as a prognostic marker in GC.

| S-EPMC7831514 | biostudies-literature

Expression analysis of colorectal cancer cell line SW480 expressing FOXC2

Project description:Investigation of whole genome gene expression level changes in a colorectal cancer cell line SW480 expressing FOXC2, compared to the pBabe control cells. Genes associated with metastasis regulated by FOXC2 in colorectal cancer were analysed. The role of FOXC2 in breast cancer metastasis are further described in Mani SA, Yang J et al. Mesenchyme Forkhead 1 (FOXC2) plays a key role in metastasis and is associated with aggressive basal-like breast cancers. PNAS 2007; 104: 10069-10074 . A six chip study using total RNA recovered from three separate cultures of SW480/pBabe and three separate cultures of SW480/FOXC2. Each chip measures the expression level of 45033 genes from SW480/pBabe or SW480/FOXC2.

2014-07-02 | E-GEOD-58980 | biostudies-arrayexpress

Expression analysis of colorectal cancer cell line SW480 expressing FOXC2

2014-07-02 | GSE58980 | GEO

Differential roles of FOXC2 in the trabecular meshwork and Schlemm’s canal in glaucomatous pathology

Project description:Impaired development and maintenance of Schlemm's canal (SC) are associated with perturbed aqueous humor outflow and intraocular pressure. The angiopoietin (ANGPT)/TIE2 signaling pathway regulates SC development and maintenance, whereas the molecular mechanisms of crosstalk between SC and the neural crest (NC)-derived neighboring tissue, the trabecular meshwork (TM), are poorly understood. Here, we show NC-specific forkhead box (Fox)c2 deletion in mice results in impaired SC morphogenesis, loss of SC identity, and elevated intraocular pressure. Visible-light optical coherence tomography analysis further demonstrated functional impairment of the SC in response to changes in intraocular pressure in NC-Foxc2 -/- mice, suggesting altered TM biomechanics. Single-cell RNA-sequencing analysis identified that this phenotype is predominately characterized by transcriptional changes associated with extracellular matrix organization and stiffness in TM cell clusters, including increased matrix metalloproteinase expression, which can cleave the TIE2 ectodomain to produce soluble TIE2. Moreover, endothelial-specific Foxc2 deletion impaired SC morphogenesis because of reduced TIE2 expression, which was rescued by deleting the TIE2 phosphatase VE-PTP. Thus, Foxc2 is critical in maintaining SC identity and morphogenesis via TM-SC crosstalk.

2023-08-29 | GSE190462 | GEO

YTHDF2 suppresses the plasmablast genetic program and promotes germinal center formation

Project description:Antibody-mediated immunity is initiated by B cell interactions with cognate antigen, followed by differentiation into multiple cell subsets, including plasmablast, memory, and germinal center (GC) cells. B cell differentiation trajectories are determined by specific transcription factors, yet very few mechanisms that determine B cell fate at the early stage of the response have been described. Here, we report an epigenetic mechanism that specifically suppresses the plasmablast genetic program and promotes GC B cell fate commitment. Single-cell RNA-seq analysis of antigen-specific B cells revealed activated B cell precursors at the pre-GC stage that express high levels of RNA binding proteins, including YTHDF2, which enhances the decay of methylated transcripts. Ythdf2-deficient B cells exhibited intact proliferation and upregulation of early activation markers in response to antigenic stimulation, whereas differentiation into GC B cells was blocked. Mechanistically, B cells required YTHDF2 to attenuate the plasmablast genetic program during GC seeding, and key transcripts of plasmablast-related genes, including Irf4 and Xbp1, were methylated and bound by YTHDF2. Modulation of YTHDF2-dependent gene expression by YTHDF1 and YTHDF3 was less pronounced, and no functional redundancy of these paralogs in GC seeding was observed. Collectively, this study reveals a novel epigenetic mechanism that specifically directs appropriate B cell fate commitment through post-transcriptional suppression of gene expression.

2022-04-24 | GSE189819 | GEO

Foxc1 and Foxc2 are necessary to maintain glomerular podocytes

Project description:Foxc1 and Foxc2 are highly expressed in adult podocytes. To bypass embryonic lethality of Foxc1 and Foxc2 KO, mice ubiquitously expressing inducible-Cre (ROSA26-CreERT2) were mated with floxed-Foxc1 and floxed-Foxc2 mice. We used microarrays to detail effects of deletions of Foxc1 and Foxc2 on podocyte gene expression profiles in adult podocyte in vivo and in vitro.

2018-07-25 | GSE117571 | GEO

FOXC2 knockdown in MDA-MB-231 cells

Project description:To determine gene expression changes in vasculogenic mimicry competent human breast cancer cells with loss of FOXC2 we performed RNA-seq of MDA-MB-231 cells with FOXC2 knockdown.

2023-07-26 | GSE232212 | GEO

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