Evidence map›Paper›PMID 36232331›Full record

ArticleInternational journal of molecular sciences2022

Tumor-Intrinsic PD-L1 Exerts an Oncogenic Function through the Activation of the Wnt/β-Catenin Pathway in Human Non-Small Cell Lung Cancer.

Yunxia Ma, Rumyana Marinkova, Miljana Nenkov, Lai Jin, Otmar Huber, Jürgen Sonnemann, Natália Peca, Nikolaus Gaßler, Yuan Chen

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 17 citations in OpenAlex.

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  3. Oncology research · 2026
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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

9 authors at 2 institutions in 2 countries.

Yunxia MaSection Pathology of the Institute of Forensic Medicine, Jena University Hospital, Friedrich Schiller University Jena, Am Klinikum 1, 07747 Jena, Germany.ORCID 0000-0001-7409-4001
Rumyana MarinkovaSection Pathology of the Institute of Forensic Medicine, Jena University Hospital, Friedrich Schiller University Jena, Am Klinikum 1, 07747 Jena, Germany.
Miljana NenkovSection Pathology of the Institute of Forensic Medicine, Jena University Hospital, Friedrich Schiller University Jena, Am Klinikum 1, 07747 Jena, Germany.ORCID 0000-0001-7976-2611
Lai JinDepartment of Hematology, Zhejiang Provincial People's Hospital, Hangzhou 310014, China.
Otmar HuberInstitute of Biochemistry II, Jena University Hospital, Friedrich Schiller University Jena, Nonnenplan 2, 07743 Jena, Germany.ORCID 0000-0003-4359-1747
Jürgen SonnemannDepartment of Pediatric Hematology and Oncology, Children's Clinic, Jena University Hospital, Friedrich Schiller University Jena, Am Klinikum 1, 07747 Jena, Germany.ORCID 0000-0003-2993-9161
Natália PecaSection Pathology of the Institute of Forensic Medicine, Jena University Hospital, Friedrich Schiller University Jena, Am Klinikum 1, 07747 Jena, Germany.
Nikolaus GaßlerSection Pathology of the Institute of Forensic Medicine, Jena University Hospital, Friedrich Schiller University Jena, Am Klinikum 1, 07747 Jena, Germany.
Yuan ChenSection Pathology of the Institute of Forensic Medicine, Jena University Hospital, Friedrich Schiller University Jena, Am Klinikum 1, 07747 Jena, Germany.ORCID 0000-0002-4752-9222
Jena University Hospital · DEZhejiang Provincial People's Hospital · CN

Funding

University Hospital Jena IZKF IZKF-MSP-06
6 · The paper itself

Abstract

Programmed death ligand 1 (PD-L1) strongly inhibits T cell activation, thereby aiding tumors in escaping the immune response. PD-L1 inhibitors have proven to be effective in the treatment of different types of cancer, including non-small cell lung cancer (NSCLC). Yet, the knowledge regarding the biological function of tumor-intrinsic PD-L1 in lung cancer remains obscure. In our study, we set the goal of determining the function of PD-L1 using overexpression and knockdown strategies. PD-L1 silencing resulted in decreased migratory and invasive ability of tumor cells, together with attenuated colony-forming capacity. Ectopic expression of PD-L1 showed the opposite effects, along with increased activities of MAPK and Wnt/β-catenin pathways, and the upregulation of Wnt/β-catenin target genes. Additionally, overexpression of PD-L1 was associated with dysregulated cellular and exosomal miRNAs involved in tumor progression and metastasis. In primary lung tumors, immunohistochemistry revealed that both PD1 and PD-L1 were highly expressed in squamous cell carcinoma (SCC) compared to adenocarcinoma (

Indexed as

Carcinoma, Non-Small-Cell LungCarcinoma, Squamous CellLung NeoplasmsMicroRNAsB7-H1 Antigenbeta CateninCarcinogenesisHumansImmune Checkpoint InhibitorsWnt Signaling PathwayB7-H1 Antigenbeta CateninCD274 protein, humanImmune Checkpoint InhibitorsMicroRNAsexosomal miRNANSCLCPD-L1Wnt/β-catenin pathway

Identifiers

PMID36232331
PMCPMC9569632
OpenAlexW4296480859

What OpenQuestion holds

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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.