Evidence map›Paper›PMID 32164050›Full record

ArticleCancer research and treatment2020

Caspase Recruitment Domain Containing Protein 9 Suppresses Non-Small Cell Lung Cancer Proliferation and Invasion via Inhibiting MAPK/p38 Pathway.

Linyue Pan, Yuting Tan, Bin Wang, Wenjia Qiu, Yulei Yin, Haiyan Ge, Huili Zhu

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

Article in Cancer research and treatment, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
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  4. Review
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

7 authors at 2 institutions in 1 country.

Linyue PanDepartment of Respiratory Medicine, The Affiliated Huadong Hospital of Fudan University, Shanghai, China.
Yuting TanDepartment of Respiratory Medicine, The Affiliated Huadong Hospital of Fudan University, Shanghai, China.
Bin WangDepartment of Thoracic Surgery, The Affiliated Huadong Hospital of Fudan University, Shanghai, China.
Wenjia QiuDepartment of Respiratory Medicine, The Affiliated Huadong Hospital of Fudan University, Shanghai, China.
Yulei YinDepartment of Pathology, The Affiliated Huadong Hospital of Fudan University, Shanghai, China.
Haiyan GeDepartment of Respiratory Medicine, The Affiliated Huadong Hospital of Fudan University, Shanghai, China.
Huili ZhuDepartment of Respiratory Medicine, The Affiliated Huadong Hospital of Fudan University, Shanghai, China.
Fudan University · CNHuadong Hospital · CN

Funding

National Natural Science Foundation of China 81600056Natural Science Foundation of Shanghai 18ZR1412 900
6 · The paper itself

Abstract

purposeCaspase recruitment domain containing protein 9 (CARD9) has been demonstrated to be a pro-tumor factor in various cancers. However, our previous study found a significant decrease of CARD9 in malignant pleural effusion compared with benign pleural effusion. So we investigated the role of CARD9 in non-small cell lung cancer (NSCLC) and its working mechanism. MATERIALS AND

methodsImmunohistochemistry, western blot, and quantitative real-time polymerase chain reaction were used to detect the expression of CARD9 in specimens of NSCLC patients. The Cancer Genome Atlas (TCGA) databasewas also used to analyze the expression of CARD9 in NSCLC and its predicting value for prognosis. Immunofluorescence was used for CARD9 cellular location. Cell growth assay, clonal formation assay, wound healing assay, matrigel invasion assay, and flow cytometry were used to test cell proliferation, migration, invasion, apoptosis, and cycle progression of NSCLC cells with CARD9 knockdown or CARD9 overexpression. Co-immunoprecipitation was used to identify the interaction between CARD9 and B-cell lymphoma 10 (BCL10). SB203580 was used to inhibit p38 activation.

resultsCARD9 was decreased in NSCLC tissues compared with normal tissues; low CARD9 expression was associated with poor survival. CARD9 was expressed both in tumor cells and macrophages. Downregulation of CARD9 in NSCLC cells enhanced the abilities of proliferation, invasion and migration via activated MAPK/p38 signaling, while overexpression of CARD9 presented antitumor effects. BCL10 was identified to interact with CARD9.

conclusionWe demonstrate that CARD9 is an independent prognostic factor in NSCLC patients and inhibits proliferation, migration, and invasion by suppressing MAPK/p38 pathway in NSCLC cells.

Indexed as

Cell ProliferationGene Expression Regulation, NeoplasticApoptosisBiomarkers, TumorCarcinoma, Non-Small-Cell LungCARD Signaling Adaptor ProteinsCell CycleCell MovementFemaleHumansLung NeoplasmsMaleMAP Kinase Signaling SystemMiddle AgedNeoplasm Invasivenessp38 Mitogen-Activated Protein KinasesBiomarkers, TumorCARD9 protein, humanCARD Signaling Adaptor Proteinsp38 Mitogen-Activated Protein KinasesCARD9Non-small cell lung cancerPrognosisTargeted therapy

Identifiers

PMID32164050
PMCPMC7373852
OpenAlexW3011776749

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.