Evidence map›Paper›PMID 29986759›Full record

ArticleJournal of experimental & clinical cancer research : CR2018

M1-like tumor-associated macrophages activated by exosome-transferred THBS1 promote malignant migration in oral squamous cell carcinoma.

Meng Xiao, Jianjun Zhang, Wanjun Chen, Wantao Chen

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
154citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 2% 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

154 citing papers in PubMed, 1 synthesis or guideline pooled it, 259 citations in OpenAlex.

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94 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 3 institutions in 2 countries.

Meng XiaoDepartment of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 639, Zhizaoju Road, Shanghai, 200011, China.
Jianjun ZhangDepartment of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 639, Zhizaoju Road, Shanghai, 200011, China.
Wanjun ChenMucosal Immunology Section, NIDCR, NIH, Bethesda, MD, 20892, USA.
Wantao ChenDepartment of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 639, Zhizaoju Road, Shanghai, 200011, China. chenwantao196323@sjtu.edu.cn.
Shanghai Jiao Tong University · CNNational Institute of Dental and Craniofacial Research · USShanghai Ninth People's Hospital · CN

Funding

TGF-beta Regulation of Mucosal and Systemic T Cell Immunity and ToleranceZIADE000101 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI CHEN, WANJUN · 2009 to 2025
$36.9M
National Natural Science Foundation of China 81472515 and 91229103National Program on Key Research Project of China 2016YFC0902700Science and Technology Commission of Shanghai Municipality 18DZ2291500
6 · The paper itself

Abstract

backgroundTreatment strategies targeting tumor-associated macrophages (TAMs) have been proposed in cancer areas. The functional alterations of macrophages in the microenvironment during the tumorigenesis of human epithelial cancer remain poorly understood. Here, we explored phenotypic alteration of macrophages during the development of oral squamous cell carcinoma (OSCC).

methodsConditioned media (CM) and exosome supernatants were harvested from normal oral epithelium, oral leukoplakia cells and OSCC cells. We measured phenotypic alteration of macrophages using flow cytometry, luminex assays, and quantitative real-time PCR assay. Intracellular signaling pathway analysis, mass spectrometry proteomics, western blotting, enzyme-linked immunosorbent assay, immunohistochemical staining, and bioinformatics analysis were performed to uncover the underlying mechanisms.

resultsTHP-1-derived and PBMCs derived macrophages exhibited an M1-like phenotype but not M2-like phenotype, when treated with CM from OSCC cells but not with the CM from normal epithelium or leukoplakia cells. Further investigations revealed that macrophages were activated by taking up exosomes released from OSCC cells through p38, Akt, and SAPK/JNK signaling at the early phase. We further provided evidences that THBS1 derived from OSCC exosomes participated in the polarization of macrophages to an M1-like phenotype. Reciprocally, CM from exosomes induced M1-like TAMs and significantly promoted migration of OSCC cells.

conclusionsWe proposed a novel paracrine loop between cancer cells and macrophages based on exosomes from OSCC. Therefore, target management of M1-like TAMs polarized by exosomes shows great potential as a therapeutic target for the control of cancerous migration in OSCC.

Indexed as

Tumor MicroenvironmentCarcinoma, Squamous CellCell Line, TumorCell MovementCell ProliferationCulture Media, ConditionedExosomesHumansImmunohistochemistryMacrophage ActivationMacrophagesMAP Kinase Signaling SystemMolecular ImagingMouth NeoplasmsThrombospondin 1Culture Media, ConditionedThrombospondin 1thrombospondin-1, humanExosomeMacrophageMigrationOral squamous cell carcinomaTHBS1

Identifiers

PMID29986759
PMCPMC6038304
OpenAlexW2827119614

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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.