Evidence map›Paper›PMID 26636733›Full record

ArticleCell cycle (Georgetown, Tex.)2016

Regulatory role of rpL3 in cell response to nucleolar stress induced by Act D in tumor cells lacking functional p53.

Annapina Russo, Valentina Pagliara, Francesco Albano, Davide Esposito, Vinay Sagar, Fabrizio Loreni, Carlo Irace, Rita Santamaria, Giulia Russo

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Review
  3. International journal of molecular sciences · 2026
    Review
  4. Review
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  6. Article
  7. Article
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  9. Article
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  11. Article
  12. Article
  13. Article
  14. Article
  15. Ribosome Biogenesis and Cancer: Overview on Ribosomal Proteins.International journal of molecular sciences · 2021
    Review
  16. Article
  17. Triangular Relationship between p53, Autophagy, and Chemotherapy Resistance.International journal of molecular sciences · 2020
    Review
  18. Review
  19. Article
  20. 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

9 authors at 3 institutions in 2 countries.

Annapina Russoa Department of Pharmacia , University of Naples "Federico II," ; Naples , Italy.
Valentina Pagliaraa Department of Pharmacia , University of Naples "Federico II," ; Naples , Italy.
Francesco Albanoa Department of Pharmacia , University of Naples "Federico II," ; Naples , Italy.
Davide Espositob Department of Molecular Medicine and Medical Biotechnology , University of Naples "Federico II," Naples , Italy.
Vinay Sagard Department of Biology , University of Rome "Tor Vergata," Rome , Italy.
Fabrizio Lorenid Department of Biology , University of Rome "Tor Vergata," Rome , Italy.
Carlo Iracea Department of Pharmacia , University of Naples "Federico II," ; Naples , Italy.
Rita Santamariaa Department of Pharmacia , University of Naples "Federico II," ; Naples , Italy.
Giulia Russoa Department of Pharmacia , University of Naples "Federico II," ; Naples , Italy.
University of Naples Federico II · ITUniversity of Rome Tor Vergata · ITIcahn School of Medicine at Mount Sinai · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many chemotherapeutic drugs cause nucleolar stress and p53-independent pathways mediating the nucleolar stress response are emerging. Here, we demonstrate that ribosomal stress induced by Actinomycin D (Act D) is associated to the up-regulation of ribosomal protein L3 (rpL3) and its accumulation as ribosome-free form in lung and colon cancer cell lines devoid of p53. Free rpL3 regulates p21 expression at transcriptional and post-translational levels through a molecular mechanism involving extracellular-signal-regulated kinases1/2 (ERK1/2) and mouse double minute-2 homolog (MDM2). Our data reveal that rpL3 participates to cell response acting as a critical regulator of apoptosis and cell migration. It is noteworthy that silencing of rpL3 abolishes the cytotoxic effects of Act D suggesting that the loss of rpL3 makes chemotherapy drugs ineffective while rpL3 overexpression associates to a strong increase of Act D-mediated inhibition of cell migration. Taking together our results show that the efficacy of Act D chemotherapy depends on rpL3 status revealing new specific targets involved in the molecular pathways activated by Act D in cancers lacking of p53. Hence, the development of treatments aimed at upregulating rpL3 may be beneficial for the treatment of these cancers.

Indexed as

Cell Line, TumorCell NucleolusCell SurvivalDactinomycinHCT116 CellsHumansRibosomal Protein L3Ribosomal ProteinsStress, PhysiologicalTumor Suppressor Protein p53DactinomycinRibosomal Protein L3Ribosomal ProteinsRPL3 protein, humanRpl3 protein, mouseTumor Suppressor Protein p53Actinomycin DapoptosiscancerERKMDM2nucleolar stressp21p53ribosomal protein

Identifiers

PMID26636733
PMCPMC4825706
OpenAlexW2192367718

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.