M6A modification profile in primary microglia with/without Igf2bp1 knockdown
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB50619 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR8314900_1.fastq.gz | Fastqsanger.gz | |||
| ERR8314900_2.fastq.gz | Fastqsanger.gz | |||
| ERR8314901_1.fastq.gz | Fastqsanger.gz | |||
| ERR8314901_2.fastq.gz | Fastqsanger.gz | |||
| ERR8314902_1.fastq.gz | Fastqsanger.gz |
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Project description:Hepatocellular carcinoma (HCC) is one of the most prevalent and lethal malignancies worldwide, with intricate molecular mechanisms driving its progression. Among various post-transcriptional regulatory mechanisms, N6-methyladenosine (m6A) modification has emerged as a critical factor influencing mRNA stability and translation, thereby impacting tumorigenesis. FK506-binding protein 9 (FKBP9), a peptidyl-prolyl isomerase (PPIase), has been implicated in several cancers; however, its specific role in HCC remains largely unexplored, and existing studies have not fully elucidated the molecular interactions and downstream effects of FKBP9 in HCC. In this study, we employed a combination of biochemical, molecular, and cellular techniques, including immunoprecipitation, RNA immunoprecipitation, luciferase reporter assays, and in vivo tumor models, to investigate the functional relationship between FKBP9 and the m6A reader protein Insulin like growth factor 2 mRNA binding protein 1 (IGF2BP1). Our findings demonstrate that FKBP9 directly interacts with IGF2BP1, enhancing its recognition of m6A-modified transcripts, particularly oncogenes such as MYC and Platelet-Derived Growth Factor Subunit B (PDGFB). Functional assays revealed that FKBP9 promotes HCC cell proliferation, migration, and invasion by stabilizing m6A-tagged oncogenic mRNAs. Furthermore, in vivo experiments confirmed that FKBP9 overexpression accelerates tumor growth, whereas MYC inhibition mitigates this effect. This study provides novel insights into the oncogenic role of FKBP9 in HCC by uncovering its regulatory influence on IGF2BP1-mediated m6A RNA recognition. These findings suggest that targeting the FKBP9-IGF2BP1 axis could be a promising therapeutic strategy for HCC.
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Project description:RNA modifications, including m6A, critically modulate protein expression program in a range of cellular processes. Although cellular senescence has been linked to age-related diseases and functional declines, the landscape and impact of m6A modification are poorly understood. Here, we report a robust m6A modification of Patched-Domain Containing Protein 4 (PTCHD4) mRNA at m6A in senescent cells. The METTL3/METTL14 complex was found to mediate the m6A modification of PTCHD4 mRNA, which increased PTCHD4 mRNA stability and PTCHD4 production. MeRIP RT-qPCR and eCLIP analyses were used to map this m6A modification to the last exon of PTCHD4 mRNA. Further investigation identified IGF2BP1, but not other m6A readers, as being responsible for stabilization and increased abundance of PTCHD4 mRNA by m6A modification. Silencing PTCHD4, a transmembrane protein, enhanced growth arrest and DNA damage in pre-senescent cells, and sensitized them to senolytic treatments and apoptosis. Our results support the notion that m6A modifications critically control senescence programs, and that factors such as METTL3/METTL14 and IGF2BP1, implicated in PTCHD4 mRNA m6A metabolism, could be exploited to eliminate senescent cells for therapeutic benefit.
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Project description:RNA modifications, including m6A, critically modulate protein expression program in a range of cellular processes. Although cellular senescence has been linked to age-related diseases and functional declines, the landscape and impact of m6A modification are poorly understood. Here, we report a robust m6A modification of Patched-Domain Containing Protein 4 (PTCHD4) mRNA at m6A in senescent cells. The METTL3/METTL14 complex was found to mediate the m6A modification of PTCHD4 mRNA, which increased PTCHD4 mRNA stability and PTCHD4 production. MeRIP RT-qPCR and eCLIP analyses were used to map this m6A modification to the last exon of PTCHD4 mRNA. Further investigation identified IGF2BP1, but not other m6A readers, as being responsible for stabilization and increased abundance of PTCHD4 mRNA by m6A modification. Silencing PTCHD4, a transmembrane protein, enhanced growth arrest and DNA damage in pre-senescent cells, and sensitized them to senolytic treatments and apoptosis. Our results support the notion that m6A modifications critically control senescence programs, and that factors such as METTL3/METTL14 and IGF2BP1, implicated in PTCHD4 mRNA m6A metabolism, could be exploited to eliminate senescent cells for therapeutic benefit.
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Project description:N6-methyl-adenosine (m6A) is the most abundant modification on messenger RNAs and is linked to human diseases, but its functions in mammalian development are poorly understood. Here we reveal the evolutionary conservation and function of m6A by mapping the m6A methylome in mouse and human embryonic stem cells. Thousands of messenger and long noncoding RNAs show conserved m6A modification, including transcripts encoding core pluripotency transcription factors. m6A is enriched over 3M-bM-^@M-^Y untranslated regions at defined sequence motifs, and marks unstable transcripts, including transcripts turned over upon differentiation. Genetic inactivation or depletion of mouse and human Mettl3, one of the m6A methylases, led to m6A erasure on select target genes, prolonged Nanog expression upon differentiation, and impaired ESCM-bM-^@M-^Ys exit from self-renewal towards differentiation into several lineages in vitro and in vivo. Thus, m6A is a mark of transcriptome flexibility required for stem cells to differentiate to specific lineages. Examing m6A modification differences in two different cell types
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