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RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1

ABSTRACT: RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1

PROVIDER: PRJNA1059024 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27384401_1.fastq.gz	Fastqsanger.gz
	SRR27384401_2.fastq.gz	Fastqsanger.gz
	SRR27384402_1.fastq.gz	Fastqsanger.gz
	SRR27384402_2.fastq.gz	Fastqsanger.gz
	SRR27384403_1.fastq.gz	Fastqsanger.gz

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RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1 [RIPK4_sh_seq]

Project description:In this study, we found that RIPK4 protein driven by TP53 mutation is highly expressed in CRC, which can promote the phosphorylation level of MTHFD1 (Methylenetetrahydrofolate Dehydrogenase, Cyclohydrolase And Formyltetrahydrofolate Synthetase 1), a key enzyme of carbon metabolism, promote the generation of NADPH in CRC cells, and reduce the level of ROS, thus promoting PANoptosis resistance and distant metastasis of CRC cells. We explain the novel mechanism of metastasis induced by the TP53 mutation in terms of post-translational modification and clarify the biological role of the RIPK4 protein in CRC, which can be used as a new target for the treatment of metastatic CRC.

2025-02-01 | GSE252263 | GEO

RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1 [Anokis_seq]

2025-02-01 | GSE252262 | GEO

RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1 [Anokis_seq]

Project description:RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1 [Anokis_seq]

| PRJNA1059030 | ENA

RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1 [RIPK4_sh_seq]

Project description:RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1 [RIPK4_sh_seq]

| PRJNA1059031 | ENA

RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-02-01 | GSE252264 | GEO

RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1

Project description:Changes in intracellular proteins of CRC cells in a suspended state

2023-12-07 | PXD047592 |

Mthfd1 is a modifier of intestinal carcinogenesis

Project description:The metabolic pathways that underlie the association between folate deficiency and increased risk for colorectal cancer (CRC) remain unclear. We have studied the effect of C1THF synthase (encoded by the Mthfd1 gene) and dietary folate and choline on intestinal tumor development in Apcmin/+ mice and azoxymethane (AOM)-induced colon cancer in mice. Mthfd1 deficiency did not alter tumor number or load in Apcmin/+ mice, but did result in a decreased incidence of colon tumors. Conversely, Mthfd1 deficiency increased tumor number 3.5-fold and tumor load 2-fold in AOM-treated mice. Here we tested colons isolated from wildtype and Mthfd1-deficient animals for alterations in gene expression. Keywords: genetic modification RNA was isolated from proximal colons of MTHFD heterozygous and wild-type mice raised on a control diet. Three colon samples were isolated from each genotype to provide biological replication.

2010-03-20 | E-GEOD-15419 | biostudies-arrayexpress

Mthfd1 is a modifier of intestinal carcinogenesis

2010-03-20 | GSE15419 | GEO

Murine MTHFD1-synthetase deficiency, a model for the human MTHFD1 R653Q polymorphism, decreases tumor growth in males

Project description:[Abstract] The R653Q variant in the synthetase domain of the folate-metabolizing enzyme MTHFD1 has been shown to increase risk for birth defects, but it does not affect risk for development of colorectal cancer (CRC). However, since we have shown that this variant reduces purine synthesis, the goal of this study was to determine whether it could affect tumor growth. Using our mouse model for MTHFD1-synthetase deficiency (Mthfd1S+/-), we induced tumor formation with azoxymethane (AOM) and dextran sodium sulfate (DSS) in male and female wild-type and Mthfd1S+/- mice. Tumor size was significantly smaller due to mutant genotype, particularly in males. Tumor size was increased in female mice compared with males, regardless of genotype. Tumor number was not influenced by genotype and was lower in females. Inflammation within tumors of male Mthfd1S+/- mice was lower than in wild-type mice. Proliferation of mouse embryonic fibroblasts from mutant lines was slower than that in wild-type fibroblasts. Gene expression analysis in tumor adjacent normal (preneoplastic) tissue identified several genes involved in proliferation (Fosb, Fos, Ptk6, Esr2, Atf3) or inflammation (Atf3, Saa1, TNF-α) that were downregulated in mutant male mice. Female mutants did not have changes in expression for those genes, nor in tumor inflammation levels, compared with wild-type, suggesting a different mechanism directing tumor growth in females. We suggest that restriction of purine synthesis and reduced expression of critical tumor-promoting genes leads to slower tumor growth in MTHFD1-synthetase deficiency. These findings may have implications for CRC tumor growth and prognosis in individuals with the R653Q variant.

2017-03-01 | GSE77931 | GEO

MTHFD1 controls DNA methylation in Arabidopsis

Project description:In order to further investigate silencing mechanisms, we screened a mutagenized Arabidopsis thaliana population for expression of SDCpro-GFP, redundantly controlled by DNA methyltransferases DRM2 and CMT3. We identified the hypomorphic mutant mthfd1-1, carrying a mutation (R175Q) in the cytoplasmic bifunctional methylenetetrahydrofolate dehydrogenase/methenyltetrahydrofolate cyclohydrolase (MTHFD1). Accumulation of homocysteine and S-adenosylhomocysteine, genome-wide DNA hypomethylation, loss of H3K9me, and transposon derepression indicate that S-adenosylmethionine-dependent transmethylation is inhibited in mthfd1-1.

2016-06-07 | GSE77966 | GEO

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