Evidence map›Paper›PMID 39240686›Full record

ArticleCancer research2024

MYC Drives mRNA Pseudouridylation to Mitigate Proliferation-Induced Cellular Stress during Cancer Development.

Jane Ding, Mohit Bansal, Yuxia Cao, Bingwei Ye, Rui Mao, Anamika Gupta, Sunil Sudarshan, Han-Fei Ding

Abstract read
In one paragraph

Article in Cancer research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed.

  1. Article
  2. Review
  3. Pseudouridine synthase 7 as a context-specific therapeutic target in cancer.The Journal of pharmacology and experimental therapeutics · 2026
    Review
  4. Article
  5. RNA modifications in cancer and their detection: a review.Japanese journal of clinical oncology · 2026
    Review
  6. TRMT6/TRMT61A-mediated tRNA mCellular & molecular biology letters · 2026
    Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
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  17. Article
  18. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Jane Ding *Department of Pathology, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.ORCID 0009-0006-3539-8145
Mohit Bansal *Department of Pathology, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.ORCID 0000-0001-8777-1980
Yuxia CaoDepartment of Pathology, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.ORCID 0009-0008-7392-7372
Bingwei YeGeorgia Cancer Center, Medical College of Georgia, Augusta University, Augusta, Georgia.ORCID 0009-0006-6865-8230
Rui MaoGeorgia Cancer Center, Medical College of Georgia, Augusta University, Augusta, Georgia.ORCID 0000-0002-6737-2939
Anamika GuptaDepartment of Pathology, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.ORCID 0009-0006-2947-9029
Sunil SudarshanO'Neal Comprehensive Cancer Center, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.ORCID 0000-0001-7257-6277
Han-Fei DingDepartment of Pathology, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.ORCID 0000-0001-5702-3439

Funding

XRAY CRYSTALLOGRAPHYP30CA013148 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Robert S Welner · 1985 to 2026
$165.9M
National Dissemination of I-Corps@NCATS: Accelerating Translation through CommercializationUL1TR003096 · NCATS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GUTIERREZ, ORLANDO M, KIMBERLY, ROBERT P. · 2019 to 2023
$43.6M
RNA epigenetic regulation of cancer metabolismR01CA190429 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI HAN-FEI DING · 2014 to 2026
$3.7M
Regulation of the Kidney Cancer Epigenome by Oncometabolite L-2-HydroxyglutarateR01CA200653 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SUNIL SUDARSHAN · 2016 to 2026
$3.6M
Reprogramming of Mitochondrial Metabolism in Renal CancerI01BX002930 · VA · BIRMINGHAM VA MEDICAL CENTER · PI SUDARSHAN, SUNIL · 2015 to 2025
–
BLRD VA I01 BX002930National Institutes of Health (NIH) R01CA190429National Institutes of Health (NIH) R01CA200653NCATS NIH HHS UL1 TR003096NCI NIH HHS P30 CA013148NCI NIH HHS R01 CA190429NCI NIH HHS R01 CA200653U.S. Department of Veterans Affairs (VA) I01BX002930
6 · The paper itself

Abstract

Pseudouridylation is a common RNA modification that is catalyzed by the family of pseudouridine synthases (PUS). Pseudouridylation can increase RNA stability and rigidity, thereby impacting RNA splicing, processing, and translation. Given that RNA metabolism is frequently altered in cancer, pseudouridylation may be a functionally important process in tumor biology. Here, we show that the MYC family of oncoproteins transcriptionally upregulates PUS7 expression during cancer development. PUS7 is essential for the growth and survival of MYC-driven cancer cells and xenografts by promoting adaptive stress responses and amino acid biosynthesis and import. ATF4, a master regulator of stress responses and cellular metabolism, was identified as a key downstream mediator of PUS7 functional activity. Induction of ATF4 by MYC oncoproteins and cellular stress required PUS7, and ATF4 overexpression overcame the growth inhibition caused by PUS7 deficiency. Mechanistically, PUS7 induced pseudouridylation of MCTS1 mRNA, which enhanced its translation. MCTS1, a noncanonical translation initiation factor, drove stress-induced ATF4 protein expression. A PUS7 consensus pseudouridylation site in the 3' untranslated region of ATF4 mRNA was crucial for the induction of ATF4 by cellular stress. These findings unveil an MYC-activated mRNA pseudouridylation program that mitigates cellular stress induced by MYC stimulation of proliferation and biomass production, suggesting that targeting PUS7 could be a therapeutic strategy selectively against MYC-driven cancers. Significance: Oncogene activation of mRNA pseudouridylation is a mechanism that facilitates metabolic reprogramming and adaptive responses to overcome cellular stress during cancer development.

Indexed as

Activating Transcription Factor 4Cell ProliferationProto-Oncogene Proteins c-mycRNA, MessengerAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansIntramolecular TransferasesMiceMice, NudeNeoplasmsPseudouridineStress, PhysiologicalActivating Transcription Factor 4ATF4 protein, humanIntramolecular TransferasesMYC protein, humanProto-Oncogene Proteins c-mycPseudouridinepseudouridine synthasesRNA, Messenger

Identifiers

PMID39240686
PMCPMC11609627

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.