Evidence map›Paper›PMID 29353287›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2018

High CXC Chemokine Ligand 16 (CXCL16) Expression Promotes Proliferation and Metastasis of Lung Cancer via Regulating the NF-κB Pathway.

Kun Liang, Yanru Liu, Dun Eer, Jingbin Liu, Fan Yang, Ke Hu

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.7field-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

33 citing papers in PubMed, 49 citations in OpenAlex.

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  16. The Role of CXCL16 in the Pathogenesis of Cancer and Other Diseases.International journal of molecular sciences · 2021
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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 3 institutions in 1 country.

Kun LiangDepartment of Respiratory Medicine, Renmin Hospital of Wuhan University, Wuhan, Hubei, China (mainland).
Yanru LiuDepartment of Respiratory Medicine, Inner Mongolia People's Hospital, Hohhot, Inner Mongolia, China (mainland).
Dun EerDepartment of Respiratory Medicine, Inner Mongolia People's Hospital, Hohhot, Inner Mongolia, China (mainland).
Jingbin LiuDepartment of Respiratory, Hospital of FIRMACO (The Fourth Affiliated Hospital of Inner Mongolia Medical University), Baotou, Inner Mongolia, China (mainland).
Fan YangDepartment of Respiratory, Hospital of FIRMACO (The Fourth Affiliated Hospital of Inner Mongolia Medical University), Baotou, Inner Mongolia, China (mainland).
Ke HuDepartment of Respiratory Medicine, Renmin Hospital of Wuhan University, Wuhan, Hubei, China (mainland).
Inner Mongolia Medical University · CNInner Mongolia People's Hospital · CNRenmin Hospital of Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND CXC chemokine ligand 16 (CXCL16) is a soluble chemokine with a transmembrane domain, playing an important role in inflammatory regulation. NF-κB has a critical role in tumor progression. Recent studies focused on the effect of CXCL16 on tumor progression. However, few reports showed the influence of CXCL16 on lung cancer, especially in regulating NF-κB activity. Here we investigated CXCL16 expression and its clinical significance in lung cancer, as well as the effect on lung cancer cell biological characteristics by regulating NF-κB. MATERIAL AND METHODS CXCL16 expression in lung cancer was detected and its associations with clinical characteristics were analyzed. Proliferation and invasion of A549 and PC-9 cells was measured before and after silencing CXCL16 or inhibiting the NF-κB pathway, separately. RESULTS The positive rate of CXCL16 in lung cancer tissue was significantly higher than that in adjacent tissue, and that in patients with lymphatic metastasis was significantly higher than that in patients without (all, P<0.05). The positive rate of CXCL16 was significantly (P<0.05) positively corrected with poor prognosis of lung cancer. Silencing CXCL16 not only suppressed proliferation and invasion of A549 and PC-9 cells, but also significantly (P<0.05) inhibited c-Rel, p105, and Rel-B in the NF-κB pathway. Inhibiting NF-κB also suppressed proliferation and invasion of A549 and PC-9 cells, which was similar to the results after silencing CXCL16. CONCLUSIONS Enhanced CXCL16 expression in lung cancer tissue promoted the proliferation and invasion of lung cancer cells. CXCL16 might promote proliferation and invasion of lung cancer by regulating the NF-κB pathway.

Indexed as

A549 CellsAdultAgedCell Line, TumorCell ProliferationChemokine CXCL16FemaleHumansLung NeoplasmsMaleMiddle AgedNeoplasm MetastasisNF-kappa BSignal TransductionSurvival RateChemokine CXCL16CXCL16 protein, humanNF-kappa B

Identifiers

PMID29353287
PMCPMC5788242
OpenAlexW2790763505

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.