Evidence map›Paper›PMID 36763655›Full record

ArticleScience advances2023

Na, K-ATPase α1 cooperates with its endogenous ligand to reprogram immune microenvironment of lung carcinoma and promotes immune escape.

Kaiyong Yang, Zijian Li, Yan Chen, Fangzhou Yin, Xiaojun Ji, Jiaqian Zhou, Xin Li, Tao Zeng, Chenghao Fei, Chenchen Ren and 8 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Steroid hormone ouabain cooperates with NaActa pharmaceutica Sinica. B · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. NaFrontiers in chemistry · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Sensational site: the sodium pump ouabain-binding site and its ligands.American journal of physiology. Cell physiology · 2024
    Review
  18. Article
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

18 authors at 2 institutions in 1 country.

Kaiyong YangState Key Laboratory of Pharmaceutical Biotechnology, College of Life Sciences, Nanjing University, Nanjing 210023, China.ORCID 0000-0001-8859-7865
Zijian LiState Key Laboratory of Pharmaceutical Biotechnology, College of Life Sciences, Nanjing University, Nanjing 210023, China.ORCID 0000-0003-0861-6726
Yan ChenState Key Laboratory of Pharmaceutical Biotechnology, College of Life Sciences, Nanjing University, Nanjing 210023, China.ORCID 0000-0002-4728-9740
Fangzhou YinSchool of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China.ORCID 0000-0003-3281-487X
Xiaojun JiState Key Laboratory of Pharmaceutical Biotechnology, College of Life Sciences, Nanjing University, Nanjing 210023, China.ORCID 0000-0002-8059-5766
Jiaqian ZhouState Key Laboratory of Pharmaceutical Biotechnology, College of Life Sciences, Nanjing University, Nanjing 210023, China.ORCID 0000-0002-2021-0027
Xin LiState Key Laboratory of Pharmaceutical Biotechnology, College of Life Sciences, Nanjing University, Nanjing 210023, China.ORCID 0000-0003-2242-777X
Tao ZengState Key Laboratory of Pharmaceutical Biotechnology, College of Life Sciences, Nanjing University, Nanjing 210023, China.ORCID 0000-0001-6805-7976
Chenghao FeiSchool of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China.ORCID 0000-0002-9575-0204
Chenchen RenSchool of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China.ORCID 0000-0002-8585-7921
Yulin WangSchool of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China.ORCID 0000-0002-5179-4643
Lei FangJiangsu Key Laboratory of Molecular Medicine, Chemistry and Biomedicine Innovation Center, Medical School of Nanjing University, Nanjing 210093, China.ORCID 0000-0002-2582-4845
Lili ChenState Key Laboratory of Pharmaceutical Biotechnology, College of Life Sciences, Nanjing University, Nanjing 210023, China.ORCID 0000-0001-8280-4229
Pei ZhangState Key Laboratory of Pharmaceutical Biotechnology, College of Life Sciences, Nanjing University, Nanjing 210023, China.ORCID 0000-0001-9038-8544
Liyan MuSchool of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China.ORCID 0000-0001-6363-9408
Yuxuan QianState Key Laboratory of Pharmaceutical Biotechnology, College of Life Sciences, Nanjing University, Nanjing 210023, China.ORCID 0000-0002-6945-6845
Yan ChenJiangsu Cancer Hospital & Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, China.ORCID 0000-0002-7149-1762
Wu YinState Key Laboratory of Pharmaceutical Biotechnology, College of Life Sciences, Nanjing University, Nanjing 210023, China.ORCID 0000-0002-5041-0134
China Pharmaceutical University · CNNanjing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulated endocrine hormones (EHs) contribute to tumorigenesis, but how EHs affect the tumor immune microenvironment (TIM) and the immunotherapy of non-small cell lung cancer (NSCLC) is still unclear. Here, endogenous ouabain (EO), an adrenergic hormone, is elevated in patients with NSCLC and closely related to tumor pathological stage, metastasis, and survival. EO promotes the suppression of TIM in vivo by modulating the expression of immune checkpoint proteins, in which programmed cell death protein ligand 1 (PD-L1) plays a major role. EO increases PD-L1 transcription; however, the EO receptor Na- and K-dependent adenosine triphosphatase (Na, K-ATPase) α1 interacts with PD-L1 to trigger the endocytic degradation of PD-L1. This seemingly contradictory result led us to discover the mechanism whereby EO cooperates with Na, K-ATPase α1 to finely control PD-L1 expression and dampen tumoral immunity. In conclusion, the Na, K-ATPase α1/EO signaling facilitates immune escape in lung cancer, and manipulation of this signaling shows great promise in improving immunotherapy for lung adenocarcinoma.

Indexed as

Adenocarcinoma of LungB7-H1 AntigenLung NeoplasmsSodium-Potassium-Exchanging ATPaseAdenosine TriphosphatasesCarcinoma, Non-Small-Cell LungHumansLigandsLungTumor MicroenvironmentAdenosine TriphosphatasesATP1A1 protein, humanB7-H1 AntigenLigandsSodium-Potassium-Exchanging ATPase

Identifiers

PMID36763655
PMCPMC9916986
OpenAlexW4320033161

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.