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MYC Promotes Cancer Progression by Modulating m6A Modification to Suppress Target Gene Translation

ABSTRACT: MYC Promotes Cancer Progression by Modulating m6A Modification to Suppress Target Gene Translation

PROVIDER: PRJNA634001 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11816542_1.fastq.gz	Fastqsanger.gz
	SRR11816542_2.fastq.gz	Fastqsanger.gz
	SRR11816543_1.fastq.gz	Fastqsanger.gz
	SRR11816543_2.fastq.gz	Fastqsanger.gz
	SRR11816544_1.fastq.gz	Fastqsanger.gz

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m6A modification regulates lung fibroblast-to-myofibroblast transition through modulating KCNH6 mRNA translation

Project description:In summary, we characterized the role of m6A modification in pulmonary fibrosis. We reveal that m6A modification is increased in bleomycin induced pulmonary fibrosis mice model, FMT-derived myofibroblasts and idiopathic pulmonary fibrosis patient lung samples. Lowering m6A level through silencing METTL3 suppress FMT process in vitro and vivo. Fundamentally, m6A modification regulates FMT by modulating the translation of KCNH6 mRNA in a YTHDF1 dependent manner. This study provides novel insights into the mechanism of FMT process and suggests m6A modification intervention may be a promising therapeutic strategy for pulmonary fibrosis.

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MYC Promotes Cancer Progression by Modulating m6A Modification to Suppress Target Gene Translation

Project description:N6-Methyladenosine (m6A) is the most prevalent internal modification in mammalian mRNAs, and participates in various fundamental bioprocesses as well as cancer. Here we immunoprecipitated m6A methylated poly (A+) RNAs (MeRIP) and then sequenced and profiled mRNA m6A methylation in P493-6 cells.

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MYC Promotes Cancer Progression by Modulating m6A Modifications to Suppress Target Gene Translation

Project description:The MYC oncoprotein activates and represses gene expression in a transcription-dependent or -independent manner. Modification of mRNA emerges as a key gene expression regulatory nexus. We sought to determine whether MYC alters mRNA modifications and report here that MYC promotes cancer progression by down-regulating N6-methyladenosine (m6A) preferentially in transcripts of a subset of MYC-repressed genes (MRGs). We find that MYC activates the expression of ALKBH5 and reduces m6A levels in the mRNA of the selected MRGs SPI1 and PHF12. We also show that MYC-regulated m6A controls the translation of MRG mRNA via the specific m6A reader YTHDF3. Finally, we find that inhibition of ALKBH5, or overexpression of SPI1 or PHF12, effectively suppresses the growth of MYC-deregulated B-cell lymphomas, both in vitro and in vivo. Our findings uncover a novel mechanism by which MYC suppresses gene expression by altering m6A modifications in selected MRG transcripts promotes cancer progression.

| S-SCDT-EMBOR-2020-51519-T | biostudies-other

m6A modification regulates lung fibroblast-to-myofibroblast transition through modulating KCNH6 mRNA translation

Project description:m6A modification regulates lung fibroblast-to-myofibroblast transition through modulating KCNH6 mRNA translation

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m6A in 5â untranslated regions promotes cap-independent translation of mRNA

Project description:N6-methyladenosine (m6A) is a widespread internal RNA modification whose function is poorly understood. Here we report that m6A residues within the 5'UTR promote a novel form of cap-independent translation which is mediated through an interaction between m6A residues and the translation initiation factor, eIF3. We present eIF3a PAR-iCLIP data which demonstrate that eIF3 predominantly binds mRNAs within the 5'UTR. eIF3 binding sites are also in proximity to m6A residues within the 5'UTR of cellular mRNAs. Two replicates of eIF3a PAR-iCLIP in HEK293T cells.

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Changes in m6A RNA methylation contribute to heart failure progression by modulating translation

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HRD1-mediated METTL14 degradation regulates m6A mRNA modification to suppress ER proteotoxic liver disease

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MYC promotes cancer progression by modulating m<sup>6</sup> A modifications to suppress target gene translation.

Project description:The MYC oncoprotein activates and represses gene expression in a transcription-dependent or transcription-independent manner. Modification of mRNA emerges as a key gene expression regulatory nexus. We sought to determine whether MYC alters mRNA modifications and report here that MYC promotes cancer progression by down-regulating N6-methyladenosine (m6 A) preferentially in transcripts of a subset of MYC-repressed genes (MRGs). We find that MYC activates the expression of ALKBH5 and reduces m6 A levels in the mRNA of the selected MRGs SPI1 and PHF12. We also show that MYC-regulated m6 A controls the translation of MRG mRNA via the specific m6 A reader YTHDF3. Finally, we find that inhibition of ALKBH5, or overexpression of SPI1 or PHF12, effectively suppresses the growth of MYC-deregulated B-cell lymphomas, both in vitro and in vivo. Our findings uncover a novel mechanism by which MYC suppresses gene expression by altering m6 A modifications in selected MRG transcripts promotes cancer progression.

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A m6A methyltransferase fine-tune m6A modification and ubiquitination to balance antiviral immunity and yield

Project description:Posttranscriptional and posttranslational modifications play crucial roles in plant immunity. However, how plant fine-tune these two modifications to activate antiviral immunity remains unknown. Here, we report that the m6A methyltransferase TaHAKAI is utilized by wheat yellow mosaic virus (WYMV) to increase viral genomic m6A modification and promotes viral replication. However, TaHAKAI also functions as an E3 ligase that targets the viral RNA silencing suppressor P2 for degradation and inhibits viral infection. A major allele of TaHAKAI in susceptible cultivar reduced the E3 ligase activity but not m6A methyltransferase activity, promoting viral infection. Interestingly, TaHAKAIR attenuates the mRNA stability of TaWPS1, the negative regulator of spike development, to increase panicle length and spikelet number by modulating its m6A modification. Our study reveals a new mechanisms of balancing disease resistance and yield by fine-tuning m6A modification and ubiquitination.

2024-10-09 | PXD056650 | Pride

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