Evidence map›Paper›PMID 36361678›Full record

ArticleInternational journal of molecular sciences2022

PTEN Loss Enhances Error-Prone DSB Processing and Tumor Cell Radiosensitivity by Suppressing RAD51 Expression and Homologous Recombination.

Xile Pei, Emil Mladenov, Aashish Soni, Fanghua Li, Martin Stuschke, George Iliakis

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

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  12. State-of-the-Art Molecular Genetics and Genomics in Germany.International journal of molecular sciences · 2023
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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 at 2 institutions in 1 country.

Xile PeiDivision of Experimental Radiation Biology, Department of Radiation Therapy, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
Emil MladenovDivision of Experimental Radiation Biology, Department of Radiation Therapy, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
Aashish SoniDivision of Experimental Radiation Biology, Department of Radiation Therapy, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.ORCID 0000-0001-9696-1006
Fanghua LiInstitute of Medical Radiation Biology, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
Martin StuschkeDivision of Experimental Radiation Biology, Department of Radiation Therapy, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
George IliakisDivision of Experimental Radiation Biology, Department of Radiation Therapy, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.ORCID 0000-0002-1152-5342
University of Duisburg-Essen · DEEssen University Hospital · DE

Funding

Deutsche Forschungsgemeinschaft GRK1739Deutsche Forschungsgemeinschaft IL51.10Deutsche Forschungsgemeinschaft IL51.11Federal Ministry for Economic Affairs and Energy 50WB1836Federal Ministry of Education and Research 02NUK037BFederal Ministry of Education and Research 02NUK043BFederal Ministry of Education and Research 02NUK054BGerman Academic Exchange Service 57515880
6 · The paper itself

Abstract

PTEN has been implicated in the repair of DNA double-strand breaks (DSBs), particularly through homologous recombination (HR). However, other data fail to demonstrate a direct role of PTEN in DSB repair. Therefore, here, we report experiments designed to further investigate the role of PTEN in DSB repair. We emphasize the consequences of PTEN loss in the engagement of the four DSB repair pathways-classical non-homologous end-joining (c-NHEJ), HR, alternative end-joining (alt-EJ) and single strand annealing (SSA)-and analyze the resulting dynamic changes in their utilization. We quantitate the effect of PTEN knockdown on cell radiosensitivity to killing, as well as checkpoint responses in normal and tumor cell lines. We find that disruption of PTEN sensitizes cells to ionizing radiation (IR). This radiosensitization is associated with a reduction in RAD51 expression that compromises HR and causes a marked increase in SSA engagement, an error-prone DSB repair pathway, while alt-EJ and c-NHEJ remain unchanged after PTEN knockdown. The G

Indexed as

DNA Breaks, Double-StrandedDNA RepairDNA End-Joining RepairHomologous RecombinationHumansPoly(ADP-ribose) Polymerase InhibitorsPTEN PhosphohydrolaseRad51 RecombinaseRadiation TolerancePoly(ADP-ribose) Polymerase InhibitorsPTEN PhosphohydrolasePTEN protein, humanRAD51 protein, humanRad51 Recombinasealt-EJc-NHEJDDRDSBsHRionizing radiationPARP inhibitorsPTENSSA

Identifiers

PMID36361678
PMCPMC9658850
OpenAlexW4307547900

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.