Evidence map›Paper›PMID 27622013›Full record

ArticleOncoimmunology2016

The proto-oncogene Myc drives expression of the NK cell-activating NKp30 ligand B7-H6 in tumor cells.

Sonja Textor, Felicitas Bossler, Kai-Oliver Henrich, Moritz Gartlgruber, Julia Pollmann, Nathalie Fiegler, Annette Arnold, Frank Westermann, Nina Waldburger, Kai Breuhahn and 3 more

Abstract read
In one paragraph

Article in Oncoimmunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
–field-weighted citation impact
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

39 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. NKp30: A Key Membrane Molecule in the Fight Against Cancer and Infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. B7 homolog 6 promotes the progression of cervical cancer.Experimental and therapeutic medicine · 2021
    Article
  17. Article
  18. Article
  19. Review
  20. 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

13 authors.

Sonja TextorInnate Immunity Group, German Cancer Research Center (DKFZ) , Heidelberg, Germany.
Felicitas BosslerInnate Immunity Group, German Cancer Research Center (DKFZ) , Heidelberg, Germany.
Kai-Oliver HenrichNeuroblastoma Genomics Group, DKFZ , Heidelberg, Germany.
Moritz GartlgruberNeuroblastoma Genomics Group, DKFZ , Heidelberg, Germany.
Julia PollmannInnate Immunity Group, German Cancer Research Center (DKFZ) , Heidelberg, Germany.
Nathalie FieglerInnate Immunity Group, German Cancer Research Center (DKFZ) , Heidelberg, Germany.
Annette ArnoldInnate Immunity Group, German Cancer Research Center (DKFZ) , Heidelberg, Germany.
Frank WestermannNeuroblastoma Genomics Group, DKFZ , Heidelberg, Germany.
Nina WaldburgerInstitute of Pathology, University Hospital Heidelberg , Heidelberg, Germany.
Kai BreuhahnInstitute of Pathology, University Hospital Heidelberg , Heidelberg, Germany.
Sven GolfierBayer HealthCare Pharmaceuticals , Berlin, Germany.
Mathias Witzens-HarigDepartment of Internal Medicine V, University of Heidelberg , Heidelberg, Germany.
Adelheid CerwenkaInnate Immunity Group, German Cancer Research Center (DKFZ) , Heidelberg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Natural Killer (NK) cells are innate effector cells that are able to recognize and eliminate tumor cells through engagement of their surface receptors. NKp30 is a potent activating NK cell receptor that elicits efficient NK cell-mediated target cell killing. Recently, B7-H6 was identified as tumor cell surface expressed ligand for NKp30. Enhanced B7-H6 mRNA levels are frequently detected in tumor compared to healthy tissues. To gain insight in the regulation of expression of B7-H6 in tumors, we investigated transcriptional mechanisms driving B7-H6 expression by promoter analyses. Using luciferase reporter assays and chromatin immunoprecipitation we mapped a functional binding site for Myc, a proto-oncogene overexpressed in certain tumors, in the B7-H6 promoter. Pharmacological inhibition or siRNA/shRNA-mediated knock-down of c-Myc or N-Myc significantly decreased B7-H6 expression on a variety of tumor cells including melanoma, pancreatic carcinoma and neuroblastoma cell lines. In tumor cell lines from different origin and primary tumor tissues of hepatocellular carcinoma (HCC), lymphoma and neuroblastoma, mRNA levels of c-Myc positively correlated with B7-H6 expression. Most importantly, upon inhibition or knock-down of c-Myc in tumor cells impaired NKp30-mediated degranulation of NK cells was observed. Thus, our data imply that Myc driven tumors could be targets for cancer immunotherapy exploiting the NKp30/B7-H6 axis.

Indexed as

B7-H6Cancer immunotherapyMycNK cellsNKp30

Identifiers

PMID27622013
PMCPMC5007025

What OpenQuestion holds

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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.