Evidence map›Paper›PMID 32457351›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2020

CCL3-CCR5 axis contributes to progression of esophageal squamous cell carcinoma by promoting cell migration and invasion via Akt and ERK pathways.

Takayuki Kodama, Yu-Ichiro Koma, Noriaki Arai, Aya Kido, Naoki Urakawa, Mari Nishio, Manabu Shigeoka, Hiroshi Yokozaki

Open access · hybridAbstract read
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

59 citing papers in PubMed, 80 citations in OpenAlex.

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  20. Inflammatory factors collaboratively linkFrontiers in immunology · 2025
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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

8 authors at 2 institutions in 1 country.

Takayuki KodamaDivision of Pathology, Department of Pathology, Kobe University Graduate School of Medicine, Kobe, Japan.
Yu-Ichiro KomaDivision of Pathology, Department of Pathology, Kobe University Graduate School of Medicine, Kobe, Japan. koma069601119@gmail.com.ORCID http://orcid.org/0000-0002-3022-8466
Noriaki AraiDivision of Pathology, Department of Pathology, Kobe University Graduate School of Medicine, Kobe, Japan.
Aya KidoDivision of Pathology, Department of Pathology, Kobe University Graduate School of Medicine, Kobe, Japan.
Naoki UrakawaDivision of Pathology, Department of Pathology, Kobe University Graduate School of Medicine, Kobe, Japan.
Mari NishioDivision of Pathology, Department of Pathology, Kobe University Graduate School of Medicine, Kobe, Japan.ORCID http://orcid.org/0000-0002-7413-0751
Manabu ShigeokaDivision of Pathology, Department of Pathology, Kobe University Graduate School of Medicine, Kobe, Japan.
Hiroshi YokozakiDivision of Pathology, Department of Pathology, Kobe University Graduate School of Medicine, Kobe, Japan.ORCID http://orcid.org/0000-0001-5276-3331
Kobe University · JPHiroshima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor-associated macrophages (TAMs) contribute to the progression and mortality of various malignancies. We reported that high numbers of infiltrating TAMs were significantly associated with tumor progression and poor prognosis in esophageal squamous cell carcinoma (ESCC). In our previous investigation of TAMs' actions in ESCC, we compared gene expression profiles between peripheral blood monocyte (PBMo)-derived macrophages and TAM-like macrophages stimulated with conditioned media of ESCC cell lines. Among the upregulated genes in the TAM-like macrophages, we focused on CC chemokine ligand 3 (CCL3), which was reported to contribute to tumor progression in several malignancies. Herein, we observed that not only TAMs but also ESCC cell lines expressed CCL3. A CCL3 receptor, CC chemokine receptor 5 (CCR5) was expressed in the ESCC cell lines. Treating the ESCC cell lines with recombinant human (rh)CCL3 induced the phosphorylations of Akt and ERK, which were suppressed by CCR5 knockdown. Migration and invasion of ESCC cells were promoted by treatment with rhCCL3 and co-culture with TAMs. TAMs/rhCCL3-promoted cell migration and invasion were suppressed by inhibition of the CCL3-CCR5 axis, PI3K/Akt, and MEK/ERK pathways. Treatment with rhCCL3 upregulated MMP2 and VEGFA expressions in ESCC cell lines. Our immunohistochemical analysis of 68 resected ESCC cases showed that high expression of CCL3 and/or CCR5 in ESCC tissues was associated with poor prognosis. High CCR5 expression was associated with deeper invasion, presence of vascular invasion, higher pathological stage, higher numbers of infiltrating CD204

Indexed as

AgedCarcinoma, Squamous CellCell Line, TumorCell MovementChemokine CCL3Disease ProgressionEsophageal NeoplasmsFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateMacrophagesMaleMAP Kinase Signaling SystemMiddle AgedChemokine CCL3Proto-Oncogene Proteins c-aktReceptors, CCR5

Identifiers

PMID32457351
PMCPMC7438203
OpenAlexW3028653052

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.