Evidence map›Paper›PMID 32632098›Full record

ArticleCell death & disease2020

PD-L1 promotes tumor growth and progression by activating WIP and β-catenin signaling pathways and predicts poor prognosis in lung cancer.

Wendan Yu, Yijun Hua, Huijuan Qiu, Jiaojiao Hao, Kun Zou, Zongjuan Li, Sheng Hu, Ping Guo, Manyu Chen, Silei Sui and 6 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed
11.1field-weighted citation impact, top 1% 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

108 citing papers in PubMed, 192 citations in OpenAlex.

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48 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

16 authors at 6 institutions in 2 countries.

Wendan Yu *Institute of Cancer Stem Cells & The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Yijun Hua *Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Huijuan Qiu *Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Jiaojiao HaoInstitute of Cancer Stem Cells & The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Kun ZouInstitute of Cancer Stem Cells & The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Zongjuan LiInstitute of Cancer Stem Cells & The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Sheng HuInstitute of Cancer Stem Cells & The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Ping GuoInstitute of Cancer Stem Cells & The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Manyu ChenInstitute of Cancer Stem Cells & The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Silei SuiInstitute of Cancer Stem Cells & The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Yuqing XiongVagelos College of Physicians and Surgeons, Columbia University, New York, NY, USA.
Fengzhou LiInstitute of Cancer Stem Cells & The First Affiliated Hospital, Dalian Medical University, Dalian, China.
Jianjun LuThe First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Wei GuoInstitute of Cancer Stem Cells & The First Affiliated Hospital, Dalian Medical University, Dalian, China. wei1015@dmu.edu.cn.
Guangyu LuoSun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China. luogy@sysucc.org.cn.
Wuguo DengSun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China. dengwg@sysucc.org.cn.
Dalian Medical University · CNFirst Affiliated Hospital of Dalian Medical University · CNSun Yat-sen University · CNSun Yat-sen University Cancer Center · CNColumbia University · USThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PD-L1 is overexpressed in tumor cells and contributes to cancer immunoevasion. However, the role of the tumor cell-intrinsic PD-L1 in cancers remains unknown. Here we show that PD-L1 regulates lung cancer growth and progression by targeting the WIP and β-catenin signaling. Overexpression of PD-L1 promotes tumor cell growth, migration and invasion in lung cancer cells, whereas PD-L1 knockdown has the opposite effects. We have also identified WIP as a new downstream target of PD-L1 in lung cancer. PD-L1 positively modulates the expression of WIP. Knockdown of WIP also inhibits cell viability and colony formation, whereas PD-L1 overexpression can reverse this inhibition effects. In addition, PD-L1 can upregulate β-catenin by inhibiting its degradation through PI3K/Akt signaling pathway. Moreover, we show that in lung cancer cells β-catenin can bind to the WIP promoter and activate its transcription, which can be promoted by PD-L1 overexpression. The in vivo experiments in a human lung cancer mouse model have also confirmed the PD-L1-mediated promotion of tumor growth and progression through activating the WIP and β-catenin pathways. Furthermore, we demonstrate that PD-L1 expression is positively correlated with WIP in tumor tissues of human adenocarcinoma patients and the high expression of PD-L1 and WIP predicts poor prognosis. Collectively, our results provide new insights into understanding the pro-tumorigenic role of PD-L1 and its regulatory mechanism on WIP in lung cancer, and suggest that the PD-L1/Akt/β-catenin/WIP signaling axis may be a potential therapeutic target for lung cancers.

Indexed as

Disease ProgressionSignal TransductionAnimalsB7-H1 Antigenbeta CateninCell Line, TumorCell MovementCell ProliferationCytoskeletal ProteinsDisease Models, AnimalEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsLung NeoplasmsMice, Inbred BALB CB7-H1 Antigenbeta CateninCytoskeletal ProteinsIntracellular Signaling Peptides and ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, MessengerWIPF1 protein, human

Identifiers

PMID32632098
PMCPMC7338457
OpenAlexW3039726497

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.