Evidence map›Paper›PMID 27020242›Full record

ArticleBMC cancer2016

Down-regulation of S100A9 inhibits osteosarcoma cell growth through inactivating MAPK and NF-κB signaling pathways.

Si Cheng, Xi Zhang, Ning Huang, Quanhe Qiu, Ying Jin, Dianming Jiang

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2016. 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
3.7field-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, 34 citations in OpenAlex.

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  5. Viral nanoparticle vaccines against S100A9 reduce lung tumor seeding and metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2023
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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

6 authors at 4 institutions in 1 country.

Si ChengDepartment of Orthopaedics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, PR China.
Xi ZhangDepartment of Nephrology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, PR China.
Ning HuangDepartment of Neurosurgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, PR China.
Quanhe QiuDepartment of Orthopaedics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, PR China.
Ying JinDepartment of Orthodontics, State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, WestChina School of Stomatology, Sichuan University, Chongqing, PR China.
Dianming JiangDepartment of Orthopaedics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, PR China. jdm571026@vip.163.com.
First Affiliated Hospital of Chongqing Medical University · CNChongqing Medical University · CNSecond Affiliated Hospital of Chongqing Medical University · CNSichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOsteosarcoma (OS) is well-known for poor prognosis due to its high incidence of proliferation and metastasis. Researches have provided valuable insights into the tumorigenesis of S100A9 in some cancers. We aimed to understand the expression level, functions and mechanisms of S100A9 in human osteosarcoma for the first time.

methodsThe expression of S100A9 protein was detected in 120 human osteosarcoma tissues and 40 normal human bone tissues using tissue microarrays analysis. The knockdown of S100A9 induced by RNA interference (RNAi) method in three osteosarcoma cell lines (U2OS, 143B, MG63) was applied to analyze the effects of S100A9 on cell proliferation, cell cycle distribution, migration, invasion and xenotransplanted tumors. Moreover, MAPK-ERK1/2, MAPK-p38, NF-κB-p65, NF-κB-p50, p21, p27, CDK2 and CDK4 were tested.

resultsThe expression of S100A9 was increased in human osteosarcoma issues and was positively correlated with clinical classification and survival rate. Down-regulation of S100A9 inhibited OS cellular proliferation, migration, invasion and cell cycle S phase in vitro and suppressed tumor formation in vivo with the reduction on PCNA and Ki67 proliferation index. Our data also demonstrated that knockdown of S100A9 repressed the protein levels of phospho-ERK1/2, phospho-p50, phospho-p65 except phospho-p38, and prompted up-regulation of p21 and p27 leading to inactivation of cyclin dependent kinase 2(CDK2) and cyclin dependent kinase 4(CDK4).

conclusionsS100A9 might be a significant role for predicting osteosarcoma prognosis and down-regulation of S100A9 could be used as a potential target for gene therapy.

Indexed as

AdultAnimalsApoptosisCalgranulin BCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMitogen-Activated Protein Kinase KinasesNF-kappa BOsteosarcomap38 Mitogen-Activated Protein KinasesSignal TransductionCalgranulin BMitogen-Activated Protein Kinase KinasesNF-kappa Bp38 Mitogen-Activated Protein KinasesInvasionMAPKNF-κBOsteosarcomaProliferationS100A9Tumorigenesis

Identifiers

PMID27020242
PMCPMC4810516
OpenAlexW2322598518

What OpenQuestion holds

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LicenceCC BY
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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.