Evidence map›Paper›PMID 25978030›Full record

ArticleOncotarget2015

Hypoxia attenuates the proinflammatory response in colon cancer cells by regulating IκB.

Kamila Müller-Edenborn, Karolin Léger, Jesus F Glaus Garzon, Carole Oertli, Ali Mirsaidi, Peter J Richards, Hubert Rehrauer, Patrick Spielmann, David Hoogewijs, Lubor Borsig and 2 more

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 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

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  7. Hypoxic stress increases NF-κB and iNOS mRNA expression in normal, but not in keratoconus corneal fibroblasts.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2021
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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

12 authors at 2 institutions in 1 country.

Kamila Müller-EdenbornInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Karolin LégerZurich Center for Integrative Human Physiology (ZIHP), University of Zurich, Zurich, Switzerland.
Jesus F Glaus GarzonInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Carole OertliInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Ali MirsaidiZurich Center for Integrative Human Physiology (ZIHP), University of Zurich, Zurich, Switzerland.
Peter J RichardsZurich Center for Integrative Human Physiology (ZIHP), University of Zurich, Zurich, Switzerland.
Hubert RehrauerFunctional Genomics Center, University of Zurich, Zurich, Switzerland.
Patrick SpielmannInstitute of Physiology, University of Zurich, Zurich, Switzerland.
David HoogewijsInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Lubor BorsigInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Michael O HottigerZurich Center for Integrative Human Physiology (ZIHP), University of Zurich, Zurich, Switzerland.
Roland H WengerInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Swiss Integrative Center for Human Health · CHUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Two main features common to all solid tumors are tissue hypoxia and inflammation, both of which cause tumor progression, metastasis, therapy resistance and increased mortality. Chronic inflammation is associated with increased cancer risk, as demonstrated for inflammatory bowel disease patients developing colon cancer. However, the interplay between hypoxia and inflammation on the molecular level remains to be elucidated. We found that MC-38 mouse colon cancer cells contain functional hypoxic (HIF-1α) and inflammatory (p65/RelA) signaling pathways. In contrast to cells of the myeloid lineage, HIF-1α levels remained unaffected in MC-38 cells treated with LPS, and hypoxia failed to induce NF-κB. A similar regulation of canonical HIF and NF-κB target genes confirmed these results. RNA deep sequencing of HIF-1α and p65/RelA knock-down cells revealed that a surprisingly large fraction of HIF target genes required p65/RelA for hypoxic regulation and a number of p65/RelA target genes required HIF-1α for proinflammatory regulation, respectively. Hypoxia attenuated the inflammatory response to LPS by inhibiting nuclear translocation of p65/RelA independently of HIF-1α, which was associated with enhanced IκBα levels and decreased IKKβ phosphorylation. These data demonstrate that the interaction between hypoxic and inflammatory signaling pathways needs to be considered when designing cancer therapies targeting HIF or NF-κB.

Indexed as

Cell HypoxiaColonic NeoplasmsHumansI-kappa B ProteinsInflammationInflammatory Bowel DiseasesLipopolysaccharidesNF-kappa BSignal TransductionI-kappa B Proteinslipopolysaccharide ALipopolysaccharidesNF-kappa Binflammatory bowel diseaselipopolysaccharideNF-κBtissue oxygenationtumor hypoxia

Identifiers

PMID25978030
PMCPMC4653005
OpenAlexW1958066496

What OpenQuestion 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 OpenQuestion graph.