Evidence map›Paper›PMID 26979829›Full record

ArticleCell and tissue research2016

Mesenchymal-epithelial signalling in tumour microenvironment: role of high-mobility group Box 1.

Sikander Sharma, Andrew Evans, Elaine Hemers

Open access · hybridAbstract read
In one paragraph

Article in Cell and tissue research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
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  9. RAGE Inhibitors for Targeted Therapy of Cancer: A Comprehensive Review.International journal of molecular sciences · 2022
    Review
  10. Comparison of Diagnostic Reliability of p63 and Smooth Muscle Actin in Salivary Gland Neoplasms.Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India · 2022
    Article
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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

3 authors at 1 institution in 1 country.

Sikander SharmaBiomolecular Sciences, School of Pharmacy and Bimolecular Sciences, Liverpool John Moores University, Liverpool, L3 3AF, UK.
Andrew EvansBiomolecular Sciences, School of Pharmacy and Bimolecular Sciences, Liverpool John Moores University, Liverpool, L3 3AF, UK.
Elaine HemersBiomolecular Sciences, School of Pharmacy and Bimolecular Sciences, Liverpool John Moores University, Liverpool, L3 3AF, UK. a.r.evans@ljmu.ac.uk.
Liverpool John Moores University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucose deprivation, hypoxia and acidosis are characteristic features of the central core of most solid tumours. Myofibroblasts are stromal cells present in many such solid tumours, including those of the colon, and are known to be involved in all stages of tumour progression. HMGB1 is a nuclear protein with an important role in nucleosome stabilisation and gene transcription; it is also released from immune cells and is involved in the inflammatory process. We report that the microenvironmental condition of glucose deprivation is responsible for the active release of HMGB1 from various types of cancer cell lines (HT-29, MCF-7 and A549) under normoxic conditions. Recombinant HMGB1 (10 ng/ml) triggered proliferation in myofibroblast cells via activation of PI3K and MEK1/2. Conditioned medium collected from glucose-deprived HT-29 colon cancer cells stimulated the migration and invasion of colonic myofibroblasts, and these processes were significantly inhibited by immunoneutralising antibodies to HMGB1, RAGE and TLR4, together with specific inhibitors of PI3K and MEK1/2. Our data suggest that HMGB1 released from cancer cells under glucose deprivation is involved in stimulating colonic myofibroblast migration and invasion and that this occurs through the activation of RAGE and TLR4, resulting in the activation of the MAPK and PI3K signalling pathways. Thus, HMGB1 might be released by cancer cells in areas of low glucose in solid tumours with the resulting activation of myofibroblasts and is a potential therapeutic target to inhibit solid tumour growth.

Indexed as

Signal TransductionTumor MicroenvironmentAdenocarcinomaAntigens, NeoplasmBlotting, WesternCell Line, TumorCell MovementCell ProliferationCollagenColonic NeoplasmsCulture Media, ConditionedDrug CombinationsEnzyme ActivationEpitheliumGlucoseHMGB1 ProteinAntigens, NeoplasmCollagenCulture Media, ConditionedDrug CombinationsGlucoseHMGB1 ProteinLamininmatrigelMitogen-Activated Protein KinasesMOK protein, humanPhosphatidylinositol 3-KinasesProteoglycansRecombinant ProteinsTLR4 protein, humanToll-Like Receptor 4Glucose deprivationHMGB1InvasionMyofibroblastsTumour microenvironment

Identifiers

PMID26979829
PMCPMC4943978
OpenAlexW2298499512

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.