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ZDHHC20-Mediated S-Palmitoylation of YTHDF3 Stabilizes MYC mRNA to Promote Pancreatic Cancer Progression

ABSTRACT: ZDHHC20-Mediated S-Palmitoylation of YTHDF3 Stabilizes MYC mRNA to Promote Pancreatic Cancer Progression

PROVIDER: PRJNA986177 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24984987_1.fastq.gz	Fastqsanger.gz
	SRR24984987_2.fastq.gz	Fastqsanger.gz
	SRR24984988_1.fastq.gz	Fastqsanger.gz
	SRR24984988_2.fastq.gz	Fastqsanger.gz
	SRR24984989_1.fastq.gz	Fastqsanger.gz

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ZDHHC20-Mediated S-Palmitoylation of YTHDF3 Stabilizes MYC mRNA to Promote Pancreatic Cancer Progression

Project description:Post-translational modifications of malignant transformation and tumor maintenance in pancreatic ductal adenocarcinoma (PDAC) in the context of KRAS signaling remains largely unexplored. Here, we used the KPC mouse model to examine the effect of palmitoylation on pancreatic cancer progression. ZDHHC20, upregulated by KRAS, is abnormally overexpressed and associated with poor prognosis in patients with pancreatic cancer. Dysregulation of ZDHHC20 promotes pancreatic cancer progression in a palmitoylation-dependent manner. ZDHHC20 inhibits lysosomal localization and degradation of YTHDF3 through S-palmitoylation of Cys474, which can result in abnormal accumulation of the oncogenic product MYC and thereby promote the malignant phenotypes of cancer cells. Further, we designed a biologically active YTHDF3-derived peptide to competitively inhibit YTHDF3 palmitoylation mediated by ZDHHC20, which in turn downregulated MYC expression and inhibited the progression of KRAS mutant pancreatic cancer. Thus, these findings highlight the therapeutic potential of targeting the ZDHHC20-YTHDF3-MYC signaling axis in pancreatic cancer.

2024-04-22 | GSE235516 | GEO

LncRNA MSAR stabilizes c-Myc to promote pancreatic cancer malignancy

Project description:LncRNA MSAR stabilizes c-Myc to promote pancreatic cancer malignancy

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LncRNA MSAR stabilizes c-Myc to promote pancreatic cancer malignancy

Project description:We identify a collection of candidate lncRNAs interacted with c-Myc in pancreatic cancer and show for the first time that an lncRNA among them, which is named as c-Myc-stabilizing and activating RNA (MSAR), promotes pancreatic cancer proliferation and metastasis through c-Myc. MSAR enhances the interaction of c-Myc and SNIP1. These findings shed light on the pro-tumorigenic role of MSAR and might provide a novel therapeutic strategy for indirect targeting c-Myc in PDAC.

2023-09-18 | GSE181777 | GEO

A palmitoylation-depalmitoylation relay spatiotemporally controls GSDMD activation in pyroptosis [I]

Project description:Gasdermin D (GSDMD) is the executioner of pyroptosis, which is important for host defense against pathogen infection. After activation, caspase-mediated cleavage of GSDMD liberates an N-terminal fragment (GSDMD-NT), which oligomerizes and forms pores in the plasma membrane, leading to cell death and subsequent release of proinflammatory cytokines. How this process is spatiotemporally controlled to promote pyroptosis in cells has been a fundamental, unaddressed question. Here, we identify GSDMD as a substrate for reversible S-palmitoylation on cysteine 192 (Cys192) in response to lipopolysaccharide (LPS) stimulation. We found that the palmitoyl acyltransferase DHHC7palmitoylates GSDMD to direct its cleavage by caspases in pyroptosis by promoting the interaction of GSDMD and caspases. We further show that after GSDMD cleavage, palmitoylation of GSDMD-NTpromotes its plasma membrane translocation and binding, and then acyl protein thioesterase 2 (APT2) depalmitoylates GSDMD-NT to unmask the Cys192 residue to promote oxidation-mediated oligomerization and pyroptosis. Perturbation of either palmitoylation or depalmitoylation suppresses pyroptosis, extends the survival of mice from LPS-induced lethal septic shock and sensitizes mice to bacterial infection. Thus. our findings reveal a model through which a palmitoylation-depalmitoylationrelay spatially and temporally controls GSDMD activation in pyroptosis.

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A palmitoylation-depalmitoylation relay spatiotemporally controls GSDMD activation in pyroptosis [II]

2024-02-25 | GSE252911 | GEO

YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis [m6A-seq]

Project description:Brain metastasis is a major cause of cancer mortality, but its molecular mechanisms are severely understudied. We found that YTHDF3 overexpression clinically correlates with brain metastases in breast cancer patients and is required for brain metastasis. Silencing YTHDF3 suppressed the brain metastasis of breast cancer cells in vitro and in vivo. Integrated transcriptome and m6A-seq analysis revealed alter expression of selected YTHDF3 target genes, including ST6GALNAC5, GJA1, and EGFR by promoting m6A-dependent translation of these target transcripts. Our work uncovers an essential role of YTHDF3 in controlling the interaction between cancer cells and brain microenvironment, thereby gaining brain metastatic competence.

2020-09-30 | GSE130172 | GEO

YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis [RIP-Seq]

2020-09-30 | GSE130171 | GEO

Transcriptome analyses of trophoblast upon YTHDF3 knockdown

Project description:YTHDF3 play important role in regulation of trophoblast activity, we examined the downstream genes of YTHDF3 via transcriptome sequencing

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ELP3 stabilizes c-Myc to promote tumorigenesis.

Project description:ELP3, the catalytic subunit of the Elongator complex, is an acetyltransferase and associated with tumor progression. However, the detail of ELP3 oncogenic function remains largely unclear. Here, we found that ELP3 stabilizes c-Myc to promote tumorigenesis in an acetyltransferase-independent manner. Mechanistically, ELP3 competes with the E3-ligase FBXW7β for c-Myc binding, resulting in the inhibition of FBXW7β-mediated ubiquitination and proteasomal degradation of c-Myc. ELP3 knockdown diminishes glycolysis and glutaminolysis and dramatically retards cell proliferation and xenograft growth by downregulating c-Myc, and such effects are rescued by the reconstitution of c-Myc expression. Moreover, ELP3 and c-Myc were found overexpressed with a positive correlation in colorectal cancer and hepatocellular carcinoma. Taken together, we elucidate a new function of ELP3 in promoting tumorigenesis by stabilizing c-Myc, suggesting that inhibition of ELP3 is a potential strategy for treating c-Myc-driven carcinomas.

| S-EPMC11054291 | biostudies-literature

Oncogenic PKA signaling stabilizes MYC oncoproteins via an aurora kinase A-dependent mechanism

Project description:Genetic alterations that activate protein kinase A (PKA) signaling are found across many tumor types, but their downstream oncogenic mechanisms are poorly understood. We used global phosphoproteomics and kinome activity profiling to map the conserved signaling outputs driven by diverse genetic changes that activate PKA in cancer. We define two consensus networks of effectors downstream of PKA in cancer models including melanoma and fibrolamellar carcinoma [FLC]. One is centered on RAS/MAPK components and a second involves Aurora Kinase A (AURKA). We find that AURKA stabilizes c-MYC and n-MYC protein levels and expression programs in PKA-dependent tumor models, in part via a positive feedback loop mediated by the oncogenic kinase PIM2. This process can be suppressed by conformation-disrupting AURKA inhibitors such as CD-532. Our findings elucidate two independent mechanisms of PKA-driven tumor cell growth and designate drug targets for study in FLC and other PKA-dependent malignancies.

2023-02-09 | PXD025508 | Pride

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