Evidence map›Paper›PMID 24813621›Full record

ArticleAutophagy2014

Autophagy promotes radiation-induced senescence but inhibits bystander effects in human breast cancer cells.

Yao-Huei Huang, Pei-Ming Yang, Qiu-Yu Chuah, Yi-Jang Lee, Yi-Fen Hsieh, Chih-Wen Peng, Shu-Jun Chiu

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 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
3.6field-weighted citation impact, top 7% 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

44 citing papers in PubMed, 78 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. ImpairedNature communications · 2026
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Senolytic effect of triterpenoid complex fromFrontiers in pharmacology · 2024
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. 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

7 authors at 4 institutions in 1 country.

Yao-Huei HuangDepartment of Life Sciences; Tzu Chi University; Hualien, Taiwan.
Pei-Ming YangThe Ph.D. Program for Cancer Biology and Drug Discovery; College of Medical Science and Technology; Taipei Medical University; Taipei, Taiwan.
Qiu-Yu ChuahDepartment of Life Sciences; Tzu Chi University; Hualien, Taiwan.
Yi-Jang LeeDepartment of Biomedical Imaging and Radiological Sciences; National Yang-Ming University; Taipei, Taiwan.
Yi-Fen HsiehDepartment of Life Sciences; Tzu Chi University; Hualien, Taiwan.
Chih-Wen PengDepartment of Life Sciences; Tzu Chi University; Hualien, Taiwan.
Shu-Jun ChiuDepartment of Life Sciences; Tzu Chi University; Hualien, Taiwan; Institute of Radiological Sciences; Tzu Chi Technology College; Hualien, Taiwan.
Hualien Tzu Chi Medical Center · TWTzu Chi University · TWNational Yang Ming Chiao Tung University · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ionizing radiation induces cellular senescence to suppress cancer cell proliferation. However, it also induces deleterious bystander effects in the unirradiated neighboring cells through the release of senescence-associated secretory phenotypes (SASPs) that promote tumor progression. Although autophagy has been reported to promote senescence, its role is still unclear. We previously showed that radiation induces senescence in PTTG1-depleted cancer cells. In this study, we found that autophagy was required for the radiation-induced senescence in PTTG1-depleted breast cancer cells. Inhibition of autophagy caused the cells to switch from radiation-induced senescence to apoptosis. Senescent cancer cells exerted bystander effects by promoting the invasion and migration of unirradiated cells through the release of CSF2 and the subsequently activation of the JAK2-STAT3 and AKT pathways. However, the radiation-induced bystander effects were correlated with the inhibition of endogenous autophagy in bystander cells, which also resulted from the activation of the CSF2-JAK2 pathway. The induction of autophagy by rapamycin reduced the radiation-induced bystander effects. This study reveals, for the first time, the dual role of autophagy in radiation-induced senescence and bystander effects.

Indexed as

Radiation, IonizingAnimalsAutophagyBreast NeoplasmsBystander EffectCell Line, TumorCell MovementCellular SenescenceChickensFemaleGranulocyte-Macrophage Colony-Stimulating FactorHumansJanus Kinase 2Models, BiologicalNeoplasm InvasivenessPhagosomesGranulocyte-Macrophage Colony-Stimulating FactorJanus Kinase 2pituitary tumor-transforming protein 1, humanProto-Oncogene Proteins c-aktSecurinSTAT3 Transcription Factorangiogenesisautophagyinvasionmigrationradiationsenescence-associated secretory phenotypes

Identifiers

PMID24813621
PMCPMC4203548
OpenAlexW2071939362

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.