Evidence map›Paper›PMID 34251762›Full record

ArticleCancer communications (London, England)2021

Nuclear Aurora kinase A triggers programmed death-ligand 1-mediated immune suppression by activating MYC transcription in triple-negative breast cancer.

Shulan Sun, Wei Zhou, Xiaoxi Li, Fei Peng, Min Yan, Yajing Zhan, Fan An, Xiaoyan Li, Yunyong Liu, Quentin Liu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer communications (London, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 50 citations in OpenAlex.

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  16. Tumor-intrinsic CDC42BPB confers resistance to anti-PD-1 immune checkpoint blockade in breast cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
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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

11 authors at 3 institutions in 1 country.

Shulan SunCentral Laboratory, Cancer Hospital of China Medical University, Dalian Medical University Clinical Oncology College, Liaoning Cancer Hospital & Institute, Shenyang, Liaoning, 110042, P. R. China.ORCID 0000-0002-7624-1797
Wei ZhouCentral Laboratory, Cancer Hospital of China Medical University, Dalian Medical University Clinical Oncology College, Liaoning Cancer Hospital & Institute, Shenyang, Liaoning, 110042, P. R. China.
Xiaoxi LiCentral Laboratory, Cancer Hospital of China Medical University, Dalian Medical University Clinical Oncology College, Liaoning Cancer Hospital & Institute, Shenyang, Liaoning, 110042, P. R. China.
Fei PengCentral Laboratory, Cancer Hospital of China Medical University, Dalian Medical University Clinical Oncology College, Liaoning Cancer Hospital & Institute, Shenyang, Liaoning, 110042, P. R. China.ORCID 0000-0003-0772-0273
Min YanState Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, 510060, P. R. China.
Yajing ZhanCentral Laboratory, Cancer Hospital of China Medical University, Dalian Medical University Clinical Oncology College, Liaoning Cancer Hospital & Institute, Shenyang, Liaoning, 110042, P. R. China.
Fan AnCentral Laboratory, Cancer Hospital of China Medical University, Dalian Medical University Clinical Oncology College, Liaoning Cancer Hospital & Institute, Shenyang, Liaoning, 110042, P. R. China.
Xiaoyan LiDepartment of Pathology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and institute, Shenyang, Liaoning, 110042, P. R. China.
Yunyong LiuDepartment of Cancer Prevention and Treatment, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang, Liaoning, 110042, P. R. China.
Quentin LiuCentral Laboratory, Cancer Hospital of China Medical University, Dalian Medical University Clinical Oncology College, Liaoning Cancer Hospital & Institute, Shenyang, Liaoning, 110042, P. R. China.ORCID 0000-0002-0999-9805
Haozhe PiaoCentral Laboratory, Cancer Hospital of China Medical University, Dalian Medical University Clinical Oncology College, Liaoning Cancer Hospital & Institute, Shenyang, Liaoning, 110042, P. R. China.
Dalian Medical University · CNSun Yat-sen University · CNLiaoning Cancer Hospital & Institute · CN

Funding

Guangdong Basic and Applied Basic Research Foundation 2018A0303130299Guangdong Basic and Applied Basic Research Foundation 2020A1515010608National Key Research and Development Program 2016YFC1303001National Natural Science Foundation of China 31801100National Natural Science Foundation of China 81630005National Natural Science Foundation of China 81702621National Natural Science Foundation of China 81703062National Natural Science Foundation of China 81820108024National Natural Science Foundation of China 81972594National Natural Science Foundation of China 82002960National Natural Science Foundation of China 82003141Natural Science Foundation of Liaoning Province 20180550618Natural Science Foundation of Liaoning Province 2019-BS-081"Seedling cultivation" program for young scientific and technological talents of Liaoning LZ2019067"Seedling cultivation" program for young scientific and technological talents of Liaoning LZ2020044
6 · The paper itself

Abstract

backgroundIncreasing studies have reported that oncogenes regulate components of the immune system, suggesting that this is a mechanism for tumorigenesis. Aurora kinase A (AURKA), a serine/threonine kinase, is involved in cell mitosis and is essential for tumor cell proliferation, metastasis, and drug resistance. However, the mechanism by which AURKA is involved in immune response regulation is unclear. Therefore, this study aimed to investigate the role of AURKA in immune regulation in triple-negative breast cancer (TNBC).

methodsPeripheral blood mononuclear cells (PBMCs) were co-cultured with TNBC cells. The xCELLigence Real-Time Cell Analyzer-MP system was used to detect the killing efficiency of immune cells on TNBC cells. The expression of immune effector molecules was tested by quantitative real-time polymerase chain reaction (qRT-PCR) to evaluate immune function. Furthermore, to validate AURKA-regulated immune response in vivo, 4T1 murine breast cancer cell line with AURKA overexpression or downregulation was engrafted into BALB/c mice. The distribution and proportion of immune cells in tumors were further evaluated by immunohistochemistry and flow cytometry.

resultsDownregulation of AURKA in TNBC cells increased immune response by activating CD8

conclusionsNuclear AURKA elevated PD-L1 expression via an MYC-dependent pathway and contributed to immune evasion in TNBC. Therapies targeting nuclear AURKA may restore immune responses against tumors.

Indexed as

B7-H1 AntigenTriple Negative Breast NeoplasmsAnimalsAurora Kinase ACD8-Positive T-LymphocytesHumansLeukocytes, MononuclearMiceMice, Inbred BALB CAurka protein, mouseAurora Kinase AB7-H1 AntigenAurora kinase Aimmune evasionimmunotherapyMYCprogrammed death-ligand 1triple-negative breast cancer

Identifiers

PMID34251762
PMCPMC8441052
OpenAlexW3180230911

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.