Evidence map›Paper›PMID 32894284›Full record

ArticleNucleic acids research2020

Hedgehog signaling enables repair of ribosomal DNA double-strand breaks.

Tshering D Lama-Sherpa, Victor T G Lin, Brandon J Metge, Shannon E Weeks, Dongquan Chen, Rajeev S Samant, Lalita A Shevde

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 32% of its field
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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Cells · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Novel role of the dietary flavonoid fisetin in suppressing rRNA biogenesis.Laboratory investigation; a journal of technical methods and pathology · 2021
    Article
  9. Article
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

7 authors at 1 institution in 1 country.

Tshering D Lama-SherpaDepartment of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA.
Victor T G LinDivision of Hematology and Oncology, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL, USA.
Brandon J MetgeDepartment of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA.
Shannon E WeeksDepartment of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA.
Dongquan ChenO'Neal Comprehensive Cancer Center, The University of Alabama at Birmingham, Birmingham, AL, USA.
Rajeev S SamantDepartment of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA.
Lalita A ShevdeDepartment of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA.
University of Alabama at Birmingham · US

Funding

XRAY CRYSTALLOGRAPHYP30CA013148 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Robert S Welner · 1985 to 2026
$165.9M
Dietary intervention of non-classical Wnt signalingR01CA194048 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SAMANT, RAJEEV S · 2016 to 2020
$1.7M
Mechanisms of resistance to cancer therapeuticsR01CA169202 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SHEVDE, LALITA A. · 2014 to 2018
$1.5M
Research Training Program in Basic and Translational OncologyT32CA183926 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BHATIA, RAVI · 2014 to 2018
$1.0M
BLRD VA I01 BX003374NCI NIH HHS P30 CA013148NCI NIH HHS R01 CA169202NCI NIH HHS R01 CA194048NCI NIH HHS T32 CA183926
6 · The paper itself

Abstract

Ribosomal DNA (rDNA) consists of highly repeated sequences that are prone to incurring damage. Delays or failure of rDNA double-strand break (DSB) repair are deleterious, and can lead to rDNA transcriptional arrest, chromosomal translocations, genomic losses, and cell death. Here, we show that the zinc-finger transcription factor GLI1, a terminal effector of the Hedgehog (Hh) pathway, is required for the repair of rDNA DSBs. We found that GLI1 is activated in triple-negative breast cancer cells in response to ionizing radiation (IR) and localizes to rDNA sequences in response to both global DSBs generated by IR and site-specific DSBs in rDNA. Inhibiting GLI1 interferes with rDNA DSB repair and impacts RNA polymerase I activity and cell viability. Our findings tie Hh signaling to rDNA repair and this heretofore unknown function may be critically important in proliferating cancer cells.

Indexed as

Cell Cycle ProteinsCell NucleolusCell ProliferationCell SurvivalDNA Breaks, Double-StrandedDNA DamageDNA RepairDNA, RibosomalGene Expression RegulationHedgehog ProteinsHumansRadiation, IonizingRibosomesRNA Polymerase ISignal TransductionTranscription, GeneticCell Cycle ProteinsDNA, RibosomalGLI1 protein, humanHedgehog ProteinsRNA Polymerase IZinc Finger Protein GLI1

Identifiers

PMID32894284
PMCPMC7544215
OpenAlexW3084116367

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

None linked

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.