Evidence map›Paper›PMID 28099922›Full record

ArticleOncotarget2017

PAFR selectively mediates radioresistance and irradiation-induced autophagy suppression in prostate cancer cells.

Bing Yao, Bingqian Liu, Lei Shi, Xiang Li, Chuanchuan Ren, Mingbo Cai, Wen Wang, Jianhua Li, Yongde Sun, Yudong Wu and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
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  8. Debris-stimulated tumor growth: a Pandora's box?Cancer metastasis reviews · 2021
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  9. Article
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  12. Review
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  14. LncRNA HULC mediates radioresistance via autophagy in prostate cancer cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018
    Article
  15. 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

11 authors at 1 institution in 1 country.

Bing YaoDepartment of Urology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Bingqian LiuDepartment of Urology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Lei ShiDepartment of Urology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Xiang LiDepartment of Plastic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Chuanchuan RenDepartment of Urology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Mingbo CaiDepartment of Gynaecology and Obstetrics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Wen WangDepartment of Gynaecology and Obstetrics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Jianhua LiDepartment of Urology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yongde SunDepartment of Urology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yudong WuDepartment of Urology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Jianguo WenDepartment of Urology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Platelet-activating factor receptor (PAFR) promotes tumorigenesis, angiogenesis and metastasis. Here, we defined the PAFR as a yielding new inhibiting target to selectively enhance the sensitivity of prostate cancer (PCa) cells to radiation. The selective responding to PAFR inhibiter may be caused by the differential expression pattern of PAFR in PCa cells. In this study, we also determined PAFR as a molecular basis by which the radiation induces autophagy suppression independent of activating mTOR pathway. PAFR can bind to the autophagy-indispensable protein Beclin 1, leading to the disability in its serine phosphorylation. The PAFR antagonist Ginkgolide B (GB) can sensitize radiotherapy by disrupting the formation of PAFR/Beclin 1 complex in PC3 and LNCaP cells, which have elevated PAFR expression after radiation exposure. Most importantly, GB efficiently radiosensitized PC3 and LNCaP tumor xenografts in vivo, and significantly reduced tumor burden. Overall, our results elucidated a significant role of GB in selectively improving the outcomes of PCa receiving radiation therapy.

Indexed as

AnimalsApoptosisBlotting, WesternCell Line, TumorFlow CytometryGinkgolidesHumansImmunoprecipitationLactonesMaleMiceMice, Inbred NODMice, SCIDPlatelet Membrane GlycoproteinsPolymerase Chain ReactionProstatic Neoplasmsginkgolide BGinkgolidesLactonesplatelet activating factor receptorPlatelet Membrane GlycoproteinsRadiation-Sensitizing AgentsReceptors, G-Protein-Coupledautophagydrug sensitivityplatelet activating factor receptorprostatic neoplasmsradiotherapy

Identifiers

PMID28099922
PMCPMC5355143
OpenAlexW2577052642

What Socratic 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 Socratic graph.