Evidence map›Paper›PMID 32860047›Full record

ArticleThe Journal of experimental medicine2020

β-Catenin induces transcriptional expression of PD-L1 to promote glioblastoma immune evasion.

Linyong Du, Jong-Ho Lee, Hongfei Jiang, Chengde Wang, Silu Wang, Zhihong Zheng, Fei Shao, Daqian Xu, Yan Xia, Jing Li and 8 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed, 1 pooled it
8.8field-weighted citation impact, top 2% 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

145 citing papers in PubMed, 1 synthesis or guideline pooled it, 226 citations in OpenAlex.

  1. Pooled it
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  15. Integrin αvβ3 is a Potential Therapeutic Target in Cholangiocarcinoma.International journal of medical sciences · 2026
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  16. Review
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  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 10 institutions in 3 countries.

Linyong DuKey Laboratory of Laboratory Medicine, Ministry of Education of China, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Jong-Ho LeeDepartment of Biological Sciences, Dong-A University, Busan, Republic of Korea.
Hongfei JiangThe Affiliated Hospital of Qingdao University, Qingdao Cancer Institute, Qingdao, Shandong, China.
Chengde WangDepartment of Neurosurgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Silu WangKey Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Zhihong ZhengDepartment of Respiratory Medicine, Sir Run Run Shaw Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Fei ShaoThe Affiliated Hospital of Qingdao University, Qingdao Cancer Institute, Qingdao, Shandong, China.
Daqian XuDepartment of Hepatobiliary and Pancreatic Surgery and Zhejiang Provincial Key Laboratory of Pancreatic Disease of The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Yan XiaBrain Tumor Center and Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX.
Jing LiState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, China.
Yanhua ZhengBrain Tumor Center and Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX.
Xu QianDepartment of Nutrition and Food Hygiene, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.
Xinjian LiChinese Academy of Sciences Key Laboratory of Infection and Immunity, Chinese Academy of Sciences Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Hyung-Ryong KimCollege of Dentistry, Dankook University, Cheonan, Republic of Korea.
Dongming XingThe Affiliated Hospital of Qingdao University, Qingdao Cancer Institute, Qingdao, Shandong, China.
Pengyuan LiuDepartment of Respiratory Medicine, Sir Run Run Shaw Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Zhimin LuDepartment of Hepatobiliary and Pancreatic Surgery and Zhejiang Provincial Key Laboratory of Pancreatic Disease of The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Jianxin LyuKey Laboratory of Laboratory Medicine, Ministry of Education of China, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Qingdao University · CNThe University of Texas MD Anderson Cancer Center · USWenzhou Medical University · CNSir Run Run Shaw Hospital · CNZhejiang University · CNChinese Academy of Sciences · CNDankook University · KRDong-A University · KRJiangsu Cancer Hospital · CNSichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PD-L1 up-regulation in cancer contributes to immune evasion by tumor cells. Here, we show that Wnt ligand and activated EGFR induce the binding of the β-catenin/TCF/LEF complex to the CD274 gene promoter region to induce PD-L1 expression, in which AKT activation plays an important role. β-Catenin depletion, AKT inhibition, or PTEN expression reduces PD-L1 expression in tumor cells, enhances activation and tumor infiltration of CD8+ T cells, and reduces tumor growth, accompanied by prolonged mouse survival. Combined treatment with a clinically available AKT inhibitor and an anti-PD-1 antibody overcomes tumor immune evasion and greatly inhibits tumor growth. In addition, AKT-mediated β-catenin S552 phosphorylation and nuclear β-catenin are positively correlated with PD-L1 expression and inversely correlated with the tumor infiltration of CD8+ T cells in human glioblastoma specimens, highlighting the clinical significance of β-catenin activation in tumor immune evasion.

Indexed as

AllograftsAnimalsAntibodiesB7-H1 Antigenbeta CateninCD8-Positive T-LymphocytesCell Line, TumorGlioblastomaHeterocyclic Compounds, 3-RingHumansLymphocyte ActivationMaleMiceMice, Inbred C57BLProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseAntibodiesB7-H1 Antigenbeta CateninCD274 protein, humanCTNNB1 protein, humanHeterocyclic Compounds, 3-RingMK 2206Proto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID32860047
PMCPMC7596815
OpenAlexW3081630303

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.