Evidence map›Paper›PMID 32468028›Full record

Observational studyInternational journal of oncology2020

The TLR4/ERK/PD‑L1 axis may contribute to NSCLC initiation.

Xiuhua Kang, Penghui Li, Chuibin Zhang, Yunshan Zhao, Huoli Hu, Guilan Wen

Open access · hybridAbstract readObservational Study
In one paragraph

Observational study in International journal of oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

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  6. Inverse Regulation of TLR4 and PD-L1 Shapes the Inflammatory Tumor Microenvironment in Oral Squamous Cell Carcinomas.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2025
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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.

Xiuhua Kang *Department of Pulmonary and Critical Care, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Penghui Li *Department of Pulmonary and Critical Care, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Chuibin ZhangDepartment of Respiratory medicine, The First Affiliated Hospital of Gannan Medical College, Ganzhou, Jiangxi 341000, P.R. China.
Yunshan ZhaoDepartment of Pulmonary and Critical Care, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Huoli HuDepartment of Thoracic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Guilan WenDepartment of Pulmonary and Critical Care, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
First Affiliated Hospital of Nanchang University · CNNanchang University · CNFirst Affiliated Hospital of Gannan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infection and inflammation serve an important role in tumor development. Toll‑like receptor 4 (TLR4) is a pivotal component of the innate and adaptive immune response during infection and inflammation. Programmed‑death ligand 1 (PD‑L1) is hypothesized as an important factor for non‑small cell lung cancer (NSCLC) immune escape. In the present study, the relationship between TLR4 and PD‑L1, in addition to the associated molecular mechanism, were investigated. TLR4 and PD‑L1 expression in lung cancer tissues were detected using immunohistochemistry, whilst overall patient survival was measured using the Kaplan‑Meier method. The A549 cell line stimulated using lipopolysaccharide (LPS) was applied as the in vitro inflammatory NSCLC model. Associated factors were investigated using reverse transcription‑quantitative PCR and western blotting. Lung cancer tissues exhibited increased PD‑L1 and TLR4 levels compared with those of adjacent para‑cancerous tissues, where there was a positive correlation between TLR4 and PD‑L1 expression. In addition, increased expression of these two proteins was found to be linked with poorer prognoses. Following the stimulation of A549 cells with LPS, TLR4 and PD‑L1 expression levels were revealed to be upregulated in a dose‑dependent manner, where the ERK and PI3K/AKT signaling pathways were found to be activated. Interestingly, in the presence of inhibitors of these two pathways aforementioned, upregulation of PD‑L1 expression was only inhibited by the MEK inhibitor PD98059, which can inhibit ERK activity. These data suggested that the ERK signaling pathway is necessary for the TLR4/PD‑L1 axis. In conclusion, data from the present study suggest that TLR4 and PD‑L1 expression can serve as important prognostic factors for NSCLC, where TLR4 activation may induce PD‑L1 expression through the ERK signaling pathway.

Indexed as

A549 CellsB7-H1 AntigenCarcinogenesisCarcinoma, Non-Small-Cell LungFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticHumansImmunohistochemistryKaplan-Meier EstimateLipopolysaccharidesLungLung NeoplasmsMaleMAP Kinase Signaling SystemMiddle AgedAKT1 protein, humanB7-H1 AntigenCD274 protein, humanLipopolysaccharidesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTLR4 protein, humanToll-Like Receptor 4inflammationinitiationnon‑small cell lung cancerprogrammed death‑ligand 1toll‑like receptor 4

Identifiers

PMID32468028
PMCPMC7307593
OpenAlexW3026700594

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.