Evidence map›Paper›PMID 26513172›Full record

ArticleOncotarget2015

Celecoxib increases lung cancer cell lysis by lymphokine-activated killer cells via upregulation of ICAM-1.

Melina Schellhorn, Maria Haustein, Marcus Frank, Michael Linnebacher, Burkhard Hinz

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Antitumor effects of valdecoxib on hypopharyngeal squamous carcinoma cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022
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  4. Review
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  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Drug repurposing in malignant pleural mesothelioma: a breath of fresh air?European respiratory review : an official journal of the European Respiratory Society · 2018
    Review
  12. Acetylsalicylic Acid Governs the Effect of Sorafenib inClinical cancer research : an official journal of the American Association for Cancer Research · 2018
    Article
  13. Review
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

5 authors at 1 institution in 1 country.

Melina SchellhornInstitute of Toxicology and Pharmacology, Rostock University Medical Center, Rostock, Germany.
Maria HausteinInstitute of Toxicology and Pharmacology, Rostock University Medical Center, Rostock, Germany.
Marcus FrankElectron Microscopy Center, Rostock University Medical Center, Rostock, Germany.
Michael LinnebacherSection of Molecular Oncology and Immunotherapy, Department of General Surgery, Rostock University Medical Center, Rostock, Germany.
Burkhard HinzInstitute of Toxicology and Pharmacology, Rostock University Medical Center, Rostock, Germany.
University of Rostock · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The antitumorigenic mechanism of the selective cyclooxygenase-2 (COX-2) inhibitor celecoxib is still a matter of debate. Using lung cancer cell lines (A549, H460) and metastatic cells derived from a lung cancer patient, the present study investigates the impact of celecoxib on the expression of intercellular adhesion molecule 1 (ICAM-1) and cancer cell lysis by lymphokine-activated killer (LAK) cells. Celecoxib, but not other structurally related selective COX-2 inhibitors (i.e., etoricoxib, rofecoxib, valdecoxib), was found to cause a substantial upregulation of ICAM-1 protein levels. Likewise, ICAM-1 mRNA expression was increased by celecoxib. Celecoxib enhanced the susceptibility of cancer cells to be lysed by LAK cells with the respective effect being reversed by a neutralizing ICAM-1 antibody. In addition, enhanced killing of celecoxib-treated cancer cells was reversed by preincubation of LAK cells with an antibody to lymphocyte function associated antigen 1 (LFA-1), suggesting intercellular ICAM-1/LFA-1 crosslink as crucial event within this process. Finally, celecoxib elicited no significant increase of LAK cell-mediated lysis of non-tumor bronchial epithelial cells, BEAS-2B, associated with a far less ICAM-1 induction as compared to cancer cells. Altogether, our data demonstrate celecoxib-induced upregulation of ICAM-1 on lung cancer cells to be responsible for intercellular ICAM-1/LFA-1 crosslink that confers increased cancer cell lysis by LAK cells. These findings provide proof for a novel antitumorigenic mechanism of celecoxib.

Indexed as

CelecoxibCell Line, TumorCyclooxygenase 2 InhibitorsHumansIntercellular Adhesion Molecule-1Killer Cells, Lymphokine-ActivatedLung NeoplasmsTransfectionUp-RegulationCelecoxibCyclooxygenase 2 InhibitorsICAM1 protein, humanIntercellular Adhesion Molecule-1celecoxibimmune surveillanceintercellular adhesion molecule 1lung cancer cellslymphokine-activated killer cells

Identifiers

PMID26513172
PMCPMC4770776
OpenAlexW2173799933

What OpenQuestion holds

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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.