Evidence map›Paper›PMID 27086923›Full record

ArticleOncogene2016

Tumor-infiltrating monocytes/macrophages promote tumor invasion and migration by upregulating S100A8 and S100A9 expression in cancer cells.

S Y Lim, A E Yuzhalin, A N Gordon-Weeks, R J Muschel

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

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 2 pooled it
10.3field-weighted citation impact, top 1% 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

123 citing papers in PubMed, 2 syntheses or guidelines pooled it, 181 citations in OpenAlex.

  1. Calprotectin (S100A8/S100A9): a key protein between inflammation and cancer.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
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  18. The roles of tissue resident macrophages in health and cancer.Experimental hematology & oncology · 2024
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63 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

S Y LimCRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford, Oxford, UK.
A E YuzhalinCRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford, Oxford, UK.
A N Gordon-WeeksCRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford, Oxford, UK.
R J MuschelCRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford, Oxford, UK.
CRUK/MRC Oxford Institute for Radiation Oncology · GBUniversity of Oxford · GB

Funding

Cancer Research UK 20407Cancer Research UK A11563
6 · The paper itself

Abstract

Myeloid cells promote the development of distant metastases, but little is known about the molecular mechanisms underlying this process. Here we have begun to uncover the effects of myeloid cells on cancer cells in a mouse model of liver metastasis. Monocytes/macrophages, but not granulocytes, isolated from experimental liver metastases stimulated migration and invasion of MC38 colon and Lewis lung carcinoma cells. In response to conditioned media from tumor-infiltrating monocytes/macrophages, cancer cells upregulated S100a8 and S100a9 messenger RNA expression through an extracellular signal-related kinase-dependent mechanism. Suppression of S100A8 and S100A9 in cancer cells using short hairpin RNA significantly diminished migration and invasion in culture. Downregulation of S100A8 and S100A9 had no effect on subcutaneous tumor growth. However, colony size was greatly reduced in liver metastases with decreased invasion into adjacent tissue. In tissue culture and in the liver colonies derived from cancer cells with knockdown of S100A8 and S100A9, MMP2 and MMP9 expression was decreased, consistent with the reduction in migration and invasion. Our findings demonstrate that monocytes/macrophages in the metastatic liver microenvironment induce S100A8 and S100A9 in cancer cells, and that these proteins are essential for tumor cell migration and invasion. S100A8 and S100A9, however, are not responsible for stimulation of proliferation. This study implicates S100A8 and S100A9 as important mediators of tumor cell aggressiveness, and highlights the therapeutic potential of S100A8 and S100A9 for interference of metastasis.

Indexed as

Gene Expression Regulation, NeoplasticCalgranulin ACalgranulin BCell Line, TumorCell MovementCell ProliferationExtracellular Signal-Regulated MAP KinasesGene Knockdown TechniquesHumansMacrophagesMonocytesMyeloid CellsNeoplasmsUp-RegulationCalgranulin ACalgranulin BExtracellular Signal-Regulated MAP Kinases

Identifiers

PMID27086923
PMCPMC4961254
OpenAlexW2338022509

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.