Evidence map›Paper›PMID 32297484›Full record

ArticleThoracic cancer2020

Aspirin-targeted PD-L1 in lung cancer growth inhibition.

Yixiang Zhang, Changsheng Lv, Yan Dong, Qingkai Yang

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 19% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Prophylactic and therapeutic effects of aspirin in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  6. The impact of aspirin on PD-L1 expression and alteration of M2 polarization in non-small cell lung cancer.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 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

4 authors at 1 institution in 1 country.

Yixiang ZhangDepartment of Thoracic Surgery, The First Affiliated Hospital of Dalian Medicine University, Dalian, China.
Changsheng LvDepartment of Thoracic Surgery, The First Affiliated Hospital of Dalian Medicine University, Dalian, China.
Yan DongDepartment of Oncology, The First Affiliated Hospital of Dalian Medical University, Dalian, China.
Qingkai YangDepartment of Cancer Stem Cell, Dalian Medicine University, Dalian, China.ORCID 0000-0002-2512-3512
Dalian Medical University · CN

Funding

Funding of natural science foundation of Liaoning province, china 20180550106
6 · The paper itself

Abstract

backgroundAspirin is a classic anti-inflammatory drug and its anticancer effect has been previously explored in many types of cancer including colorectal cancer therapy. Programmed cell death-ligand 1 (PD-L1) is widely expressed in tumor cells and displays an inhibitory role in antitumor immunity. This study aimed to clarify the role of PD-L1 in aspirin-suppressed lung cancer.

methodsThe inhibitory effect of aspirin on lung cancer cell proliferation was assessed using an MTT cell viability assay. The role of aspirin in the modulation of PD-L1 expression was analyzed by western blot or RT-PCR assays. In lung cancer cells, the influence of aspirin on PD-L1 promoter activity was detected using a luciferase reporter assay. The interaction of TAZ with PD-L1 promoter in the cells, with or without aspirin administration, was tested via chromatin immunoprecipitation (ChIP) analysis. The function of PD-L1 in aspirin-mediated growth inhibition of lung cancer was examined using a cell viability assay.

resultsFollowing treatment with aspirin, lung cancer cell growth was markedly suppressed. Aspirin was able to markedly decrease the expression of PD-L1 at the mRNA and protein levels in lung cancer cells. For the mechanism study, we found that the promoter of PD-L1 was inactivated by aspirin via TAZ transcriptional coactivator in the cells. With regard to the functional investigation, aspirin was capable of resisting cell proliferation and PD-L1 overexpression abolished aspirin-depressed cell proliferation in lung cancer.

conclusionsAspirin suppressed the growth of lung cancer cells via targeting the TAZ/PD-L1 axis.

Indexed as

Anti-Inflammatory Agents, Non-SteroidalAspirinB7-H1 AntigenCell ProliferationGene Expression Regulation, NeoplasticHumansLung NeoplasmsTumor Cells, CulturedAnti-Inflammatory Agents, Non-SteroidalAspirinB7-H1 AntigenCD274 protein, humanAspiringrowthlung cancerPD-L1TAZ

Identifiers

PMID32297484
PMCPMC7262895
OpenAlexW3016280519

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.