Evidence map›Paper›PMID 33208183›Full record

ArticleJournal of experimental & clinical cancer research : CR2020

Evodiamine suppresses non-small cell lung cancer by elevating CD8

Ze-Bo Jiang, Ju-Min Huang, Ya-Jia Xie, Yi- Zhong Zhang, Chan Chang, Huan-Ling Lai, Wenjun Wang, Xiao-Jun Yao, Xing-Xing Fan, Qi-Biao Wu and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 2 pooled it
5.1field-weighted citation impact, top 3% 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

73 citing papers in PubMed, 2 syntheses or guidelines pooled it, 114 citations in OpenAlex.

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13 more citing papers are in PubMed but not listed here.

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

13 authors at 3 institutions in 2 countries.

Ze-Bo JiangState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Macao, Taipa Macau (SAR), China.
Ju-Min HuangState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Macao, Taipa Macau (SAR), China.
Ya-Jia XieState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Macao, Taipa Macau (SAR), China.
Yi- Zhong ZhangState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Macao, Taipa Macau (SAR), China.
Chan ChangDepartment of Respiratory and Critical Care Medicine, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, China.
Huan-Ling LaiState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Macao, Taipa Macau (SAR), China.
Wenjun WangState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Macao, Taipa Macau (SAR), China.
Xiao-Jun YaoState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Macao, Taipa Macau (SAR), China.
Xing-Xing FanState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Macao, Taipa Macau (SAR), China.
Qi-Biao WuState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Macao, Taipa Macau (SAR), China.
Chun XieState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Macao, Taipa Macau (SAR), China.
Mei-Fang WangDepartment of Respiratory and Critical Care Medicine, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, China. wmfpps02@hotmail.com.
Elaine Lai-Han LeungState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Macao, Taipa Macau (SAR), China. lhleung@must.edu.mo.
Macau University of Science and Technology · MOHubei University of Medicine · CNTaihe Hospital · CN

Funding

Taihe Hospital with internal funding and the Science and Technology Development Fund Project no: 0096/2018/A3, 130/2017/A3, and 0099/2018/A3the NSFC overseas and Hong Kong and Macao Scholars Cooperative Research Fund Project Project no: 81828013The Science and Technology Development Fund, Macau SAR Project no: 0096/2018/A3
6 · The paper itself

Abstract

backgroundAccumulating evidence showed that regulating tumor microenvironment plays a vital role in improving antitumor efficiency. Programmed Death Ligand 1 (PD-L1) is expressed in many cancer cell types, while its binding partner Programmed Death 1 (PD1) is expressed in activated T cells and antigen-presenting cells. Whereas, its dysregulation in the microenvironment is poorly understood. In the present study, we confirmed that evodiamine downregulates MUC1-C, resulting in modulating PD-L1 expression in non-small cell lung cancer (NSCLC).

methodsCell viability was measured by MTT assays. Apoptosis, cell cycle and surface PD-L1 expression on NSCLC cells were analyzed by flow cytometry. The expression of MUC1-C and PD-L1 mRNA was measured by real time RT-PCR methods. Protein expression was examined in evodiamine-treated NSCLC cells using immunoblotting or immunofluorescence assays. The effects of evodiamine treatment on NSCLC sensitivity towards T cells were investigated using human peripheral blood mononuclear cells and Jurkat, apoptosis and IL-2 secretion assays. Female H1975 xenograft nude mice were used to assess the effect of evodiamine on tumorigenesis in vivo. Lewis lung carcinoma model was used to investigate the therapeutic effects of combination evodiamine and anti-PD-1 treatment.

resultsWe showed that evodiamine significantly inhibited growth, induced apoptosis and cell cycle arrest at G2 phase of NSCLC cells. Evodiamine suppressed IFN-γ-induced PD-L1 expression in H1975 and H1650. MUC1-C mRNA and protein expression were decreased by evodiamine in NSCLC cells as well. Evodiamine could downregulate the PD-L1 expression and diminish the apoptosis of T cells. It inhibited MUC1-C expression and potentiated CD8

conclusionsEvodiamine can suppress NSCLC by elevating of CD8

Indexed as

AnimalsCarcinoma, Non-Small-Cell LungCD8-Positive T-LymphocytesDown-RegulationFemaleHumansLung NeoplasmsMiceMucin-1Plant ExtractsProgrammed Cell Death 1 ReceptorQuinazolinesTransfectionevodiamineMUC1 protein, humanMucin-1Plant ExtractsProgrammed Cell Death 1 ReceptorQuinazolinesEvodiamineImmune microenvironmentMUC1-CNSCLCPD-L1

Identifiers

PMID33208183
PMCPMC7677782
OpenAlexW3101342405

What OpenQuestion holds

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LicenceCC BY
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.