Evidence map›Paper›PMID 32161124›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

Tumor cell-intrinsic PD-1 receptor is a tumor suppressor and mediates resistance to PD-1 blockade therapy.

Xiaodong Wang, Xiaohui Yang, Chang Zhang, Yang Wang, Tianyou Cheng, Liqiang Duan, Zhou Tong, Shuguang Tan, Hangjie Zhang, Phei Er Saw and 14 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed
12.0field-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

162 citing papers in PubMed, 237 citations in OpenAlex.

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102 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

24 authors at 6 institutions in 1 country.

Xiaodong WangSchool of Life Sciences, University of Science and Technology of China, 230000 Hefei, China.
Xiaohui YangSchool of Life Sciences, University of Science and Technology of China, 230000 Hefei, China.ORCID 0000-0001-5175-5209
Chang ZhangChinese Academy of Sciences (CAS) Key Laboratory of Bio-medical Diagnostics, Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, 215163 Suzhou, China.
Yang WangShanxi Academy of Advanced Research and Innovation, 030032 Taiyuan, China.
Tianyou ChengShanxi Academy of Advanced Research and Innovation, 030032 Taiyuan, China.
Liqiang DuanShanxi Academy of Advanced Research and Innovation, 030032 Taiyuan, China.
Zhou TongShanxi Academy of Advanced Research and Innovation, 030032 Taiyuan, China.
Shuguang TanCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, 100101 Beijing, China.
Hangjie ZhangCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, 100101 Beijing, China.
Phei Er SawGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 510120 Guangzhou, People's Republic of China.
Yinmin GuChinese Academy of Sciences (CAS) Key Laboratory of Bio-medical Diagnostics, Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, 215163 Suzhou, China.
Jinhua WangChinese Academy of Sciences (CAS) Key Laboratory of Bio-medical Diagnostics, Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, 215163 Suzhou, China.
Yibi ZhangChinese Academy of Sciences (CAS) Key Laboratory of Bio-medical Diagnostics, Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, 215163 Suzhou, China.
Lina ShangShanxi Academy of Advanced Research and Innovation, 030032 Taiyuan, China.
Yajuan LiuShanxi Academy of Advanced Research and Innovation, 030032 Taiyuan, China.
Siyuan JiangChinese Academy of Sciences (CAS) Key Laboratory of Bio-medical Diagnostics, Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, 215163 Suzhou, China.
Bingxue YanShanxi Academy of Advanced Research and Innovation, 030032 Taiyuan, China.
Rong LiChinese Academy of Sciences (CAS) Key Laboratory of Bio-medical Diagnostics, Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, 215163 Suzhou, China.
Yue YangDepartment of Thoracic Surgery II, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital and Institute, 100142 Beijing, China.
Jie YuDepartment of Pathology, the People's Hospital of Suzhou National Hi-Tech District, 215010 Suzhou, China.
Yunzhao ChenDepartment of Pathology, the People's Hospital of Suzhou National Hi-Tech District, 215010 Suzhou, China.
George Fu GaoShanxi Academy of Advanced Research and Innovation, 030032 Taiyuan, China; gaos@sibet.ac.cn gaof@im.ac.cn.ORCID 0000-0002-3869-615X
Qinong YeDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, 100850 Beijing, China.
Shan GaoChinese Academy of Sciences (CAS) Key Laboratory of Bio-medical Diagnostics, Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, 215163 Suzhou, China; gaos@sibet.ac.cn gaof@im.ac.cn.
Chinese Academy of Sciences · CNShanxi Academy of Building Research · CNThe Fifth People’s Hospital of Suzhou · CNUniversity of Science and Technology of China · CNPeking University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The programmed cell death 1 (PD-1) receptor on the surface of immune cells is an immune checkpoint molecule that mediates the immune escape of tumor cells. Consequently, antibodies targeting PD-1 have shown efficacy in enhancing the antitumor activity of T cells in some types of cancers. However, the potential effects of PD-1 on tumor cells remain largely unknown. Here, we show that PD-1 is expressed across a broad range of tumor cells. The silencing of PD-1 or its ligand, PD-1 ligand 1 (PD-L1), promotes cell proliferation and colony formation in vitro and tumor growth in vivo. Conversely, overexpression of PD-1 or PD-L1 inhibits tumor cell proliferation and colony formation. Moreover, blocking antibodies targeting PD-1 or PD-L1 promote tumor growth in cell cultures and xenografts. Mechanistically, the coordination of PD-1 and PD-L1 activates its major downstream signaling pathways including the AKT and ERK1/2 pathways, thus enhancing tumor cell growth. This study demonstrates that PD-1/PD-L1 is a potential tumor suppressor and potentially regulates the response to anti-PD-1/PD-L1 treatments, thus representing a potential biomarker for the optimal cancer immunotherapeutic treatment.

Indexed as

Drug Resistance, NeoplasmAnimalsAntibodies, MonoclonalApoptosisB7-H1 AntigenBiomarkers, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansLung NeoplasmsMiceMice, Inbred NODMice, SCIDProgrammed Cell Death 1 ReceptorSignal TransductionT-LymphocytesAntibodies, MonoclonalB7-H1 AntigenBiomarkers, TumorCD274 protein, humanPDCD1 protein, humanProgrammed Cell Death 1 Receptorbiomarkerdrug resistancetumor cell-intrinsic PD-1tumor cell-intrinsic PD-L1tumor suppressor

Identifiers

PMID32161124
PMCPMC7104341
OpenAlexW3011009916

What OpenQuestion holds

Textmetadata
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.