Dong et al. 2020 (PRJNA667952)
General Details
| Title | Relaxed initiation pausing of ribosomes drives oncogenic translation |
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| Organism | |
| Number of Samples | 16 |
| Release Date | 2020/10/07 00:00 |
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Study Links
| GWIPS-viz | Trips-Viz |
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Repository Details
| SRA | SRP286677 |
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| ENA | SRP286677 |
| GEO | GSE159210 |
| BioProject | PRJNA667952 |
Publication
| Title | |
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| Authors | Dong L,Mao Y,Zhou A,Liu XM,Zhou J,Wan J,Qian SB |
| Journal | Science advances |
| Publication Date | 2021 Feb |
| Abstract | Translation is a crucial process in cancer development and progression. Many oncogenic signaling pathways target the translation initiation stage to satisfy the increased anabolic demands of cancer cells. Using quantitative profiling of initiating ribosomes, we found that ribosomal pausing at the start codon serves as a 'brake' to restrain the translational output. In response to oncogenic RAS signaling, the initiation pausing relaxes and contributes to the increased translational flux. Intriguingly, messenger RNA (mRNA) m 6 A modification in the vicinity of start codons influences the behavior of initiating ribosomes. Under oncogenic RAS signaling, the reduced mRNA methylation leads to relaxed initiation pausing, thereby promoting malignant transformation and tumor growth. Restored initiation pausing by inhibiting m 6 A demethylases suppresses RAS-mediated oncogenic translation and subsequent tumorigenesis. Our findings unveil a paradigm of translational control that is co-opted by RAS mutant cancer cells to drive malignant phenotypes. Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC). |
| PMC | PMC7888950 |
| PMID | 33597240 |
| DOI |
| Run Accession | Study Accession | Scientific Name | Cell Line | Library Type | Treatment | GWIPS-viz | Trips-Viz | Reads | BAM | BigWig (F) | BigWig (R) | ||
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| SRR12790129 | PRJNA667952 | Homo sapiens | HEK-TtH cells stably expressing fused ER:HRasG12V | Ribo-Seq |  |
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| SRR12790130 | PRJNA667952 | Homo sapiens | HEK-TtH cells stably expressing fused ER:HRasG12V | Ribo-Seq | |
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| SRR12790133 | PRJNA667952 | Homo sapiens | HEK-TtH cells stably expressing fused ER:HRasG12V | Ribo-Seq | |
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| SRR12790134 | PRJNA667952 | Homo sapiens | HEK-TtH cells stably expressing fused ER:HRasG12V | Ribo-Seq | |
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| SRR12790137 | PRJNA667952 | Homo sapiens | HEK293 | Ribo-Seq | |
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| SRR12790138 | PRJNA667952 | Homo sapiens | HEK293 | Ribo-Seq | |
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| SRR12790141 | PRJNA667952 | Homo sapiens | HEK293 | Ribo-Seq | |
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| SRR12790142 | PRJNA667952 | Homo sapiens | HEK293 | Ribo-Seq | |
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| SRR12790145 | PRJNA667952 | Homo sapiens | HEK293 | Ribo-Seq | |
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| SRR12790146 | PRJNA667952 | Homo sapiens | HEK293 | Ribo-Seq | |
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| SRR12790149 | PRJNA667952 | Homo sapiens | HEK293 | Ribo-Seq | |
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| SRR12790150 | PRJNA667952 | Homo sapiens | HEK293 | Ribo-Seq | |
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| SRR12790153 | PRJNA667952 | Homo sapiens | HEK293 | Ribo-Seq | |
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| SRR12790154 | PRJNA667952 | Homo sapiens | HEK293 | Ribo-Seq | |
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| SRR12790157 | PRJNA667952 | Homo sapiens | HEK-TtH cells stably expressing fused ER:HRasG12V | Ribo-Seq | |
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| SRR12790158 | PRJNA667952 | Homo sapiens | HEK-TtH cells stably expressing fused ER:HRasG12V | Ribo-Seq | |
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| Run Accession | Study Accession | Scientific Name | Cell Line | Library Type | Treatment | GWIPS-viz | Trips-Viz | Reads | BAM | BigWig (F) | BigWig (R) |
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