Evidence map›Paper›PMID 24626185›Full record

ArticleCell cycle (Georgetown, Tex.)2014

Sustained activation of DNA damage response in irradiated apoptosis-resistant cells induces reversible senescence associated with mTOR downregulation and expression of stem cell markers.

Zhanna V Chitikova, Serguei A Gordeev, Tatiana V Bykova, Svetlana G Zubova, Valery A Pospelov, Tatiana V Pospelova

Abstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing 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

44 citing papers in PubMed.

  1. Trial
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  3. Article
  4. Therapy-induced senescent tumor cells in cancer relapse.Journal of the National Cancer Center · 2023
    Review
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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

6 authors.

Zhanna V ChitikovaInstitute of Cytology; Russian Academy of Sciences; St. Petersburg, Russia; Saint Petersburg State University; St. Petersburg, Russia.
Serguei A GordeevInstitute of Cytology; Russian Academy of Sciences; St. Petersburg, Russia; Saint Petersburg State University; St. Petersburg, Russia.
Tatiana V BykovaInstitute of Cytology; Russian Academy of Sciences; St. Petersburg, Russia; Saint Petersburg State University; St. Petersburg, Russia.
Svetlana G ZubovaInstitute of Cytology; Russian Academy of Sciences; St. Petersburg, Russia; Saint Petersburg State University; St. Petersburg, Russia.
Valery A PospelovInstitute of Cytology; Russian Academy of Sciences; St. Petersburg, Russia; Saint Petersburg State University; St. Petersburg, Russia.
Tatiana V PospelovaInstitute of Cytology; Russian Academy of Sciences; St. Petersburg, Russia; Saint Petersburg State University; St. Petersburg, Russia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cells respond to genotoxic stress by activating the DNA damage response (DDR). When injury is severe or irreparable, cells induce apoptosis or cellular senescence to prevent transmission of the lesions to the daughter cells upon cell division. Resistance to apoptosis is a hallmark of cancer that challenges the efficacy of cancer therapy. In this work, the effects of ionizing radiation on apoptosis-resistant E1A + E1B transformed cells were investigated to ascertain whether the activation of cellular senescence could provide an alternative tumor suppressor mechanism. We show that irradiated cells arrest cell cycle at G 2/M phase and resume DNA replication in the absence of cell division followed by formation of giant polyploid cells. Permanent activation of DDR signaling due to impaired DNA repair results in the induction of cellular senescence in E1A + E1B cells. However, irradiated cells bypass senescence and restore the population by dividing cells, which have near normal size and ploidy and do not express senescence markers. Reversion of senescence and appearance of proliferating cells were associated with downregulation of mTOR, activation of autophagy, mitigation of DDR signaling, and expression of stem cell markers.

Indexed as

DNA DamageAdenovirus E1A ProteinsAdenovirus E1B ProteinsApoptosisAutophagyBiomarkersCell Line, TransformedCell ProliferationCellular SenescenceDNA RepairDNA ReplicationDown-RegulationG2 Phase Cell Cycle CheckpointsHumansNanog Homeobox ProteinOctamer Transcription Factor-3Adenovirus E1A ProteinsAdenovirus E1B ProteinsBiomarkersMTOR protein, humanNanog Homeobox ProteinNanog protein, ratOctamer Transcription Factor-3TOR Serine-Threonine KinasesTranscription Factorsapoptosis resistanceautophagyDNA damage responseDNA repairmTORpolyploidysenescence reversionstem cells markers

Identifiers

PMID24626185
PMCPMC4050140

What OpenQuestion holds

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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.