Evidence map›Paper›PMID 29625612›Full record

ArticleCell communication and signaling : CCS2018

Interaction between human osteosarcoma and mesenchymal stem cells via an interleukin-8 signaling loop in the tumor microenvironment.

Masanori Kawano, Kazuhiro Tanaka, Ichiro Itonaga, Tatsuya Iwasaki, Hiroshi Tsumura

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.6field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 52 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Masanori KawanoDepartment of Orthopaedic Surgery, Faculty of Medicine, Oita University, Oita, 879-5593, Japan.
Kazuhiro TanakaDepartment of Orthopaedic Surgery, Faculty of Medicine, Oita University, Oita, 879-5593, Japan. ktanaka@oita-u.ac.jp.
Ichiro ItonagaDepartment of Orthopaedic Surgery, Faculty of Medicine, Oita University, Oita, 879-5593, Japan.
Tatsuya IwasakiDepartment of Orthopaedic Surgery, Faculty of Medicine, Oita University, Oita, 879-5593, Japan.
Hiroshi TsumuraDepartment of Orthopaedic Surgery, Faculty of Medicine, Oita University, Oita, 879-5593, Japan.
Oita University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOsteosarcoma (OS) is the representative primary malignant bone tumor with the highest incidence. It is known that malignant phenotypes of OS, such as proliferation, invasion, and metastasis, are significantly influenced not only by characteristics of the tumor itself, but also by the surrounding microenvironment. In other words, OS is considered to utilize cells in the vicinity of the tumor by changing the characteristics of these cells. Direct intercellular contact is believed to be important for this phenomenon. In the present study, we hypothesized that an interaction mediated by a humoral factor, requiring no cellular contact, might play a significant role in the progression of OS.

methodsWe developed a new co-culture model, using OS cells and mesenchymal stem cells (MSCs) without cellular contact, and found that both cell types expressed IL-8 at a high level, and FAK in OS cells was phosphorylated leading to an increase in the metastatic potential of the tumor in the co-culture condition.

resultsIt was revealed that OS cells formed a loop of signal cross-talk in which they released IL-8 as a paracrine factor, stimulating MSCs to express IL-8, and received IL-8 released by MSCs to accelerate IL-8 expression in OS cells. Administration of anti-IL-8 antibody resulted in the inhibition of FAK expression, its downstream signaling, and the invasive potential of the OS cells, resulting in decrease in metastatic lesions.

conclusionThe present study might lead not only to the clarification of a new molecular mechanism of invasion and metastasis of OS, but also to the development of a new therapeutic strategy of blocking IL-8 in OS.

Indexed as

Tumor MicroenvironmentAnimalsAntibodiesCell Line, TumorCell MovementCell ProliferationCoculture TechniquesFocal Adhesion Kinase 1HumansInterleukin-8Mesenchymal Stem CellsMiceMice, NudeNeoplasm MetastasisOsteosarcomaPhosphorylationAntibodiesFocal Adhesion Kinase 1Interleukin-8Recombinant ProteinsInterleukin-8Mesenchymal stem cellsOsteosarcomaTumor proliferation and metastasis

Identifiers

PMID29625612
PMCPMC5889532
OpenAlexW2806882608

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LicenceCC BY
Read underepoch 390

Registered trials

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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.