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YTHDF2 inhibits gastric cancer cell growth by regulating FOXC2 signaling pathway

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

PROVIDER: PRJNA680305 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13112160_1.fastq.gz	Fastqsanger.gz
	SRR13112160_2.fastq.gz	Fastqsanger.gz
	SRR13112161_1.fastq.gz	Fastqsanger.gz
	SRR13112161_2.fastq.gz	Fastqsanger.gz
	SRR13112162_1.fastq.gz	Fastqsanger.gz

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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: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: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.

2021-01-28 | GSE162004 | GEO

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

JMJD1A inhibits proliferation and aggressiveness of gastric cancer by up-regulating RUNX3

Project description:JMJD1A inhibits proliferation and aggressiveness of gastric cancer by up-regulating RUNX3

| PRJNA606040 | ENA

The tumor intrinsic role of the m6A reader YTHDF2 in regulating immune evasion [RNA-seq]

Project description:Tumors evade attacks from the immune system through various mechanisms. Here, we identify a component of tumor immune evasion mediated by YTH domain-containing family protein 2 (YTHDF2), a reader protein that usually destabilizes m6A-modified mRNA. Loss of tumoral YTHDF2 inhibits tumor growth and prolongs survival in immunocompetent tumor models. Mechanistically, tumoral YTHDF2 deficiency promotes the recruitment of macrophages via CX3CL1 and enhances mitochondrial respiration of CD8+ T cells by impairing tumor glycolysis metabolism. Tumoral YTHDF2 deficiency promotes inflammatory macrophage polarization and antigen presentation in the presence of IFN-γ. In addition, IFN-γ induces autophagic degradation of tumoral YTHDF2, thereby sensitizing tumor cells to CD8+ T cell-mediated cytotoxicity. Last, we identified a small molecule compound that preferentially induces YTHDF2 degradation, which shows a potent antitumor effect alone but a better effect when combined with anti-PD-L1 or anti-PD-1 antibodies. Collectively, YTHDF2 appears to be a tumor-intrinsic regulator that orchestrates immune evasion, representing a promising target for enhancing cancer immunotherapy.

2024-05-31 | GSE239423 | GEO

The tumor intrinsic role of the m6A reader YTHDF2 in regulating immune evasion [scRNA-seq]

2024-05-31 | GSE239426 | GEO

The tumor intrinsic role of the m6A reader YTHDF2 in regulating immune evasion [bulk RNA-seq]

2024-05-31 | GSE256058 | GEO

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

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

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