Evidence map›Paper›PMID 27958308›Full record

ArticleScientific reports2016

Protective effect of mild endoplasmic reticulum stress on radiation-induced bystander effects in hepatocyte cells.

Yuexia Xie, Shuang Ye, Jianghong Zhang, Mingyuan He, Chen Dong, Wenzhi Tu, Peifeng Liu, Chunlin Shao

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. 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
2.3field-weighted citation impact, top 12% 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, 20 citations in OpenAlex.

  1. Article
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  8. Article
  9. Vitamin BFrontiers in pharmacology · 2019
    Article
  10. Radiation, inflammation and the immune response in cancer.Mammalian genome : official journal of the International Mammalian Genome Society · 2018
    Review
  11. Article
  12. Article
  13. 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

8 authors at 2 institutions in 1 country.

Yuexia XieInstitute of Radiation Medicine, Fudan University, Shanghai, China.
Shuang YeInstitute of Radiation Medicine, Fudan University, Shanghai, China.
Jianghong ZhangInstitute of Radiation Medicine, Fudan University, Shanghai, China.
Mingyuan HeInstitute of Radiation Medicine, Fudan University, Shanghai, China.
Chen DongInstitute of Radiation Medicine, Fudan University, Shanghai, China.
Wenzhi TuInstitute of Radiation Medicine, Fudan University, Shanghai, China.
Peifeng LiuCentral Laboratory, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Chunlin ShaoInstitute of Radiation Medicine, Fudan University, Shanghai, China.
Fudan University · CNRenji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Radiation-induced bystander effect (RIBE) has important implications for secondary cancer risk assessment during cancer radiotherapy, but the defense and self-protective mechanisms of bystander normal cells are still largely unclear. The present study found that micronuclei (MN) formation could be induced in the non-irradiated HL-7702 hepatocyte cells after being treated with the conditioned medium from irradiated hepatoma HepG2 cells under either normoxia or hypoxia, where the ratio of the yield of bystander MN induction to the yield of radiation-induced MN formation under hypoxia was much higher than that of normoxia. Nonetheless, thapsigargin induced endoplasmic reticulum (ER) stress and dramatically suppressed this bystander response manifested as the decrease of MN and apoptosis inductions. Meanwhile, the interference of BiP gene, a major ER chaperone, amplified the detrimental RIBE. More precisely, thapsigargin provoked ER sensor of PERK to initiate an instantaneous and moderate ER stress thus defensed the hazard form RIBE, while BiP depletion lead to persistently destroyed homeostasis of ER and exacerbated cell injury. These findings provide new insights that the mild ER stress through BiP-PERK-p-eIF2α signaling pathway has a profound role in protecting cellular damage from RIBE and hence may decrease the potential secondary cancer risk after cancer radiotherapy.

Indexed as

Endoplasmic Reticulum StressActivating Transcription Factor 6ApoptosisBystander EffectCell HypoxiaCulture Media, ConditionedeIF-2 KinaseEndoplasmic Reticulum Chaperone BiPEnzyme InhibitorsEukaryotic Initiation Factor-2Heat-Shock ProteinsHepatocytesHep G2 CellsHumansSignal TransductionThapsigarginActivating Transcription Factor 6ATF6 protein, humanCulture Media, ConditionedEIF2AK3 protein, humaneIF-2 KinaseEndoplasmic Reticulum Chaperone BiPEnzyme InhibitorsEukaryotic Initiation Factor-2Heat-Shock ProteinsThapsigarginX-Box Binding Protein 1XBP1 protein, human

Identifiers

PMID27958308
PMCPMC5153638
OpenAlexW2567015563

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.