Evidence map›Paper›PMID 29259270›Full record

ArticleScientific reports2017

IFNγ induces PD-L1 overexpression by JAK2/STAT1/IRF-1 signaling in EBV-positive gastric carcinoma.

Ji Wook Moon, Su-Kang Kong, Byung Soo Kim, Hyun Ji Kim, Hyangsoon Lim, Kyeonga Noh, Younghye Kim, Jung-Woo Choi, Ju-Han Lee, Young-Sik Kim

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

110 citing papers in PubMed, 155 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Do Metastatic Cells Arise from PD-L1International journal of molecular sciences · 2026
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

50 more citing papers are in PubMed but not listed here.

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

10 authors at 1 institution in 2 countries.

Ji Wook MoonDepartment of Pathology, Korea University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0003-1384-1469
Su-Kang KongDepartment of Pathology, Korea University College of Medicine, Seoul, Republic of Korea.
Byung Soo KimDepartment of Pathology, Korea University College of Medicine, Seoul, Republic of Korea.
Hyun Ji KimDepartment of Pathology, Korea University College of Medicine, Seoul, Republic of Korea.
Hyangsoon LimDepartment of Pathology, Korea University College of Medicine, Seoul, Republic of Korea.
Kyeonga NohDepartment of Pathology, Korea University College of Medicine, Seoul, Republic of Korea.
Younghye KimDepartment of Pathology, Korea University Ansan Hospital, Ansan, Republic of Korea.
Jung-Woo ChoiDepartment of Pathology, Korea University Ansan Hospital, Ansan, Republic of Korea.
Ju-Han LeeDepartment of Pathology, Korea University Ansan Hospital, Ansan, Republic of Korea.
Young-Sik KimDepartment of Pathology, Korea University College of Medicine, Seoul, Republic of Korea. apysk@korea.ac.kr.
Korea University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Programmed death-ligand 1 (PD-L1) acts as an immune checkpoint inhibitor in various cancers. PD-L1 is known to be more frequently expressed in EBV (+) gastric cancer (GC). However, the mechanisms underlying the regulation of PD-L1 expression in EBV (+) GC remain unclear. We investigated the basal and inducible PD-L1 expressions in GC cells. PD-L1 expression was upregulated upon treatment with IFNγ in both EBV (-) and EBV (+) GC cells. Upon stimulation with the same concentration of IFNγ for 24 h, EBV (+) SNU-719 cells showed dramatically higher PD-L1 expression levels by activating JAK2/STAT1/IRF-1 signaling than those of EBV (-) AGS cells. PD-L1 promoter assays, chromatin immunoprecipitation, and electrophoretic mobility shift assays revealed that IFNγ-inducible PD-L1 overexpression is primarily mediated by the putative IRF-1α site of the PD-L1 promoter in EBV (+) SNU-719 cells. Moreover, EBNA1 knockdown reduced both constitutive and IFNγ-inducible PD-L1 promoter activity by decreasing the transcript and protein levels of JAK2 and subsequently STAT1/IRF-1/PD-L1 signaling. EBNA1 is suggested to be moderately enhance both constitutive and IFNγ-inducible PD-L1 expression in EBV (+) GC cells. Thus, the signaling proteins and EBNA1 that regulate PD-L1 expression are potential therapeutic targets in EBV (+) GC.

Indexed as

B7-H1 AntigenCell Line, TumorEpstein-Barr Virus InfectionsGene Expression Regulation, NeoplasticHerpesvirus 4, HumanHumansInterferon-gammaInterferon Regulatory Factor-1Janus Kinase 2ProteinsSignal TransductionSTAT1 Transcription FactorStomach NeoplasmsB7-H1 AntigenCD274 protein, humanInterferon-gammaInterferon Regulatory Factor-1IRF1 protein, humanJAK2 protein, humanJanus Kinase 2ProteinsSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID29259270
PMCPMC5736657
OpenAlexW2773629709

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.