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Nonsense-mediated mRNA Decay

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The Upf proteins that carry out nonsense-mediated decay (NMD) are found in all eukaryotic organisms, including humans. Each protein has an individual role, but they need to work in collaboration. Upf1 is an ATP-dependent RNA helicase that unwinds the RNA helix. Because Upf1 can unwind any RNA, Upf2 and Upf3 are required to help Upf1 discriminate between nonsense and normal mRNAs.
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During most eukaryotic translation processes, the small 40S ribosome subunit scans an mRNA from its 5' end until it encounters the first start AUG codon. The large 60S ribosomal subunit then joins the smaller one to initiate protein synthesis. The location of the translation initiation is largely determined by the nucleotides near the start codon as there may be multiple translation initiation sites present on the mRNA.  Marilyn Kozak discovered that the sequence RCCAUGG (where R...
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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The nucleolus is the most prominent substructure of the nucleus. When it was first discovered, it was considered to be an isolated organelle that forms fibrils and granules. In 1931, the relationship between the nucleolus and chromosomes was first described by Heitz. He observed that the appearance and size of nucleolus varies depending on the stage of the cell cycle. He also noticed constricted regions on different chromosomes clustered together at definite cell cycle stages. These regions,...
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Initiating translation is complex because it involves multiple molecules. Initiator tRNA, ribosomal subunits, and eukaryotic initiation factors (eIFs) are all required to assemble on the initiation codon of mRNA. This process consists of several steps that are mediated by different eIFs.
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The structure and stability of mRNA molecules regulates gene expression, as mRNAs are a key step in the pathway from gene to protein. In eukaryotes, the half-life of mRNA varies from a few minutes up to several days. mRNA stability is essential in growth and development. The absence of the proteins regulating its stability, such as tristetraprolin in mice, can cause systemic issues, including bone marrow overgrowth, inflammation, and autoimmunity.
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Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis
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EcDNA-borne PVT1 fusion stabilizes oncogenic mRNAs.

Hyerim Yi, Shu Zhang, Jason Swinderman

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    Extrachromosomal DNA (ecDNA) amplifications drive cancer by creating gene fusions. The PVT1-MYC fusion, stabilized by PVT1 exon 1, enhances oncogene activity and cancer progression.

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    Area of Science:

    • Oncology
    • Molecular Biology
    • Genomics

    Background:

    • Extrachromosomal DNA (ecDNA) amplifications are key drivers in human cancers.
    • ecDNA structural variants frequently lead to oncogenic gene fusions.

    Purpose of the Study:

    • Investigate the role of ecDNA structural variants in cancer.
    • Characterize the function of PVT1-MYC fusions in cancer development.

    Main Methods:

    • Analysis of cancer genomes for structural variants on ecDNA.
    • Mechanistic studies on PVT1 exon 1 and SRSF1 interaction.
    • Genetic rescue experiments in MYC-addicted cancer models.
    • Single-cell RNA sequencing of tumors.

    Main Results:

    • PVT1 is the most recurrent structural variant on ecDNA, frequently forming PVT1-MYC fusions.
    • PVT1 exon 1 stabilizes fusion transcripts by interacting with SRSF1.
    • PVT1-MYC fusions enhance MYC dependency and activate MYC target genes in vivo.

    Conclusions:

    • ecDNA instability generates oncogenic lncRNA-mRNA fusions.
    • PVT1 exon 1 acts as a key stabilizer for oncogene mRNAs, promoting cancer.
    • Targeting PVT1-MYC fusions may offer new therapeutic strategies.