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Regulation of hepatocellular carcinoma growth by UPF1 variants not through nonsense-mediated mRNA decay

ABSTRACT: Multiple studies showed that overexpression of UPF1 reduced the growth of HCC. However, it remains unanswered how UPF1 expression retarded HCC proliferation. Thus, this study employed UPF1 variants to evaluate the UPF1 function in HCC growth inhibition. Transcriptome analysis indicated that the level of DUSP1, dual specificity phosphatase 1, was upregulated by UPF1 variants by posttranscriptional regulation. The increase of DUPS1 by UPF1 overexpression repressed the downstream signaling, inhibiting cell growth.

ORGANISM(S): Homo sapiens

PROVIDER: GSE185655 | GEO | 2021/10/13

REPOSITORIES: GEO

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Target discrimination in nonsense-mediated mRNA decay requires Upf1 ATPase activity (CLIP-Seq)

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Target discrimination in nonsense-mediated mRNA decay requires Upf1 ATPase activity (RIP-Seq)

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Target discrimination in nonsense-mediated mRNA decay requires Upf1 ATPase activity (RIP-Seq)

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The origins and consequences of UPF1 variants in pancreatic adenosquamous carcinoma

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Regulation of hepatocellular carcinoma growth by UPF1 variants not through nonsense-mediated mRNA decay

Project description:Regulation of hepatocellular carcinoma growth by UPF1 variants not through nonsense-mediated mRNA decay

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Global analysis of Upf1 in mESCs reveals expanded scope of nonsense-mediated mRNA decay

Project description:Nonsense-mediated mRNA decay (NMD) is a conserved RNA surveillance pathway that is an important modulator of disease pathology and is required for embryonic development. Despite significant research effort, the rules that govern NMD remain incompletely understood. Here we used a combined¬ approach, integrating RNA-Seq, ribosome footprinting, and CLIP-Seq analysis of the essential NMD factor Upf1, to provide a more complete picture of the role of NMD in modulating gene expression in murine embryonic stem cells (mESCs). We show that presence of an exon-exon junction ?50 nucleotides (nt) downstream of a termination codon (dEJ) contributes to NMD independently of 3' UTR length, but has stronger effects in genes with shorter 3' UTRs. We also map translated upstream open reading frames (uORFs) in mESCs and show that they are associated with NMD regulation, especially of genes encoding transcription factors, and we find that lowly translated mRNAs can escape NMD. Finally, we identify over 200 direct binding targets of Upf1 and describe a pathway of Upf1-dependent gene regulation reliant on Upf1 binding to the 3' UTR and independent of presence of a dEJ. Together, these analyses characterize known and discover novel determinants of NMD and establish a broader role in mESC gene regulation for Upf1. mRNA-Seq analysis of wildtype (2 samples), translationally inhibited (by cycloheximide treatment, 2 samples), control-depleted (2 samples), and Upf1-depleted (4 samples) mouse embryonic stem cells (mESCs); CLIP-Seq analysis of Upf1 (5 samples, and 5 samples of IgG control CLIP-Seq); Ribosome footprint profiling of wildtype (1 sample), control-depleted (1 sample), and Upf1-depleted (1 sample) mESCs

2013-06-12 | E-GEOD-41785 | biostudies-arrayexpress

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2013-06-12 | GSE41785 | GEO

PTBP1 excludes UPF1 to protect long 3'UTRs from nonsense-mediated mRNA decay

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