Evidence map›Paper›PMID 28326700›Full record

ArticleHua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology2016

[In vitro investigation on the mechanism of cyclooxygenase-2 upregulation induced by spleen tyrosine kinase-nuclear factor κB signaling in cancer pain caused by oral cancer-associated macrophage].

Lin Jie, Wang Miao, Ji Yang, Liu Le, Gao Pan, Li Chunjie

Open access · greenAbstract read
In one paragraph

Article in Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 72% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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 1 institution in 1 country.

Lin JieState Key Laboratory of Oral Diseases, Dept. of Dental Anesthesia, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China.
Wang MiaoState Key Laboratory of Oral Diseases, Dept. of Dental Anesthesia, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China.
Ji YangState Key Laboratory of Oral Diseases, Dept. of Dental Anesthesia, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China.
Liu LeState Key Laboratory of Oral Diseases, Dept. of Dental Anesthesia, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China.
Gao PanState Key Laboratory of Oral Diseases, Dept. of Head and Neck Oncology, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China.
Li ChunjieState Key Laboratory of Oral Diseases, Dept. of Head and Neck Oncology, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China.
Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis study explores the mechanism of cyclooxygenase-2 (COX-2) upregulation in oral cancers associated with macrophage by using molecular biology techniques and primary culture of murine macrophage.

methodsMurine macrophage was induced by macrophage colony-stimulating factor (M-CSF) and Cal27 conditional medium (CM). Purity of the macrophage was detected through CD68 immunofluorescence staining. Inhibitors of spleen tyrosine kinase (Syk) and nuclear factor κB (NFκB) were used to inhibit these pathways. In addition, real-time polymerase chain reaction and Western blot analysis were used to detect alterations in COX-2 and pathway-related proteins.

resultsAll of the induced cells specifically expressed CD68. Cal27 CM could significantly induce COX-2 expression (P<0.001). Moreover, inhibition of Syk pathway attenuated NFκB-P65 phosphorylation and reduced COX-2 expression (P<0.01), and inhibition of NFκB pathway exerted no effects on Syk phosphorylation but significantly inhibited COX-2 upregulation (P<0.01).

conclusionsSyk-NFκB is responsible for COX-2 overexpression in oral cancer associated with macrophages. Targeting this pathway is possibly a new approach to control oral cancer-related pain.
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Indexed as

Cancer PainMacrophagesMouth NeoplasmsSignal TransductionAnimalsCyclooxygenase 2Macrophage Colony-Stimulating FactorMiceNF-kappa BPhosphorylationSpleenSyk KinaseUp-RegulationCyclooxygenase 2Macrophage Colony-Stimulating FactorNF-kappa BPtgs2 protein, mouseSyk KinaseSyk protein, mousecancer paincyclooxygenase-2macrophagemouth neoplasm

Identifiers

PMID28326700
PMCPMC7030122
OpenAlexW3013835279

What OpenQuestion holds

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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.