Evidence map›Paper›PMID 28572836›Full record

ArticleInfectious agents and cancer2017

LPS promotes resistance to TRAIL-induced apoptosis in pancreatic cancer.

Katharina Beyer, Lars Ivo Partecke, Felicitas Roetz, Herbert Fluhr, Frank Ulrich Weiss, Claus-Dieter Heidecke, Wolfram von Bernstorff

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Infectious agents and cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Pyroptosis in acute pancreatitis and its therapeutic regulation.Apoptosis : an international journal on programmed cell death · 2022
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. 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

7 authors at 2 institutions in 1 country.

Katharina Beyer *Department of General, Visceral, Thoracic and Vascular Surgery, Universitätsmedizin Greifswald, Greifswald, Germany.
Lars Ivo Partecke *Department of General, Visceral, Thoracic and Vascular Surgery, Universitätsmedizin Greifswald, Greifswald, Germany.
Felicitas Roetz *Department of General, Visceral, Thoracic and Vascular Surgery, Universitätsmedizin Greifswald, Greifswald, Germany.
Herbert FluhrDepartment of Medicine A, Universitätsmedizin Greifswald, Greifswald, Germany.
Frank Ulrich WeissDepartment of Obstetrics and Gynaecology, Universitätsklinikum Heidelberg, Heidelberg, Germany.
Claus-Dieter HeideckeDepartment of General, Visceral, Thoracic and Vascular Surgery, Universitätsmedizin Greifswald, Greifswald, Germany.
Wolfram von BernstorffDepartment of General, Visceral, Thoracic and Vascular Surgery, Universitätsmedizin Greifswald, Greifswald, Germany.
Universitätsmedizin Greifswald · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThough TRAIL has been hailed as a promising drug for tumour treatment, it has been observed that many tumour cells have developed escape mechanisms against TRAIL-induced apoptosis. As a receptor of LPS, TLR 4, which is expressed on a variety of cancer cells, can be associated with TRAIL-resistance of tumour cells and tumour progression as well as with the generation of an anti-tumour immune response.

methodsIn this study, the sensitivity to TRAIL-induced apoptosis as well as the influence of LPS-co-stimulation on the cell viability of the pancreatic cancer cell lines PANC-1, BxPC-3 and COLO 357 was examined by FACS analyses and a cell viability assay. Subsequently, the expression of TRAIL-receptors was detected via FACS analyses. Levels of osteoprotegerin (OPG) were also determined using an enzyme-linked immunosorbent assay.

resultsPANC-1 cells were shown to be resistant to TRAIL-induced apoptosis. This was accompanied by significantly increased osteoprotegerin levels and a significantly decreased expression of DR4. In contrast, TRAIL significantly induced apoptosis in COLO 357 cells and to a lesser degree in BxPC-3 cells. Co-stimulation of COLO 357 as well as BxPC-3 cells combining TRAIL and LPS resulted in a significant decrease in TRAIL-induced apoptosis. In COLO 357 cells TRAIL-stimulation decreased the levels of OPG thereby not altering the expression of the TRAIL-receptors 1-4 resulting in a high susceptibility to TRAIL-induced apoptosis. Co-stimulation with LPS and TRAIL completely reversed the effect of TRAIL on OPG levels reaching a 2-fold increase beyond the level of non-stimulated cells resulting in a lower susceptibility to apoptosis. In BxPC-3, TRAIL stimulation decreased the expression of DR4 and significantly increased the decoy receptors TRAIL-R3 and TRAIL-R4 leading to a decrease in TRAIL-induced apoptosis. OPG levels remained unchanged. Co-stimulation with TRAIL and LPS further enhanced the changes in TRAIL-receptor-expression promoting apoptosis resistance.

conclusionsHere it has been shown that TRAIL-resistance in pancreatic cancer cells can be mediated by the inflammatory molecule LPS as well as by different expression patterns of functional and non-functional TRAIL-receptors.

Indexed as

ApoptosisCell linesLPSPancreas cancerTRAIL

Identifiers

PMID28572836
PMCPMC5450120
OpenAlexW2617059091

What OpenQuestion holds

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LicenceCC BY
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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.