Evidence map›Paper›PMID 41428871›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2025

A PSAT1 buff of YBX1 transcriptionally sustains HLA-E-mediated evasion of NK immunity.

Yangyi Zhang, He Ren, Chaobing Ma, Changhong Shi, Ruigang Yang, Chenxi Wang, Pengfei Feng, Bo Zhang, Chenyu Liu, Zubiao Niu and 8 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. A PSAT1 buff of YBX1 transcriptionally sustains HLA-E-mediated evasion of NK immunity.Proceedings of the National Academy of Sciences of the United States of America · 2025
    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.

Yangyi Zhang *Department of Oncology, Beijing Shijitan Hospital, Capital Medical University, Beijing 10038, China.
He Ren *Department of Oncology, Beijing Shijitan Hospital, Capital Medical University, Beijing 10038, China.ORCID 0009-0002-7553-7331
Chaobing Ma *Department of Oncology, Beijing Shijitan Hospital, Capital Medical University, Beijing 10038, China.ORCID 0000-0001-6143-2374
Changhong Shi *Laboratory Animal Center, Air Force Medical University, Xi'an 710032, China.
Ruigang YangAcademy of Military Medical Science, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, Beijing 100071, China.ORCID 0000-0002-1048-9298
Chenxi WangAcademy of Military Medical Science, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, Beijing 100071, China.
Pengfei FengAcademy of Military Medical Science, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, Beijing 100071, China.ORCID 0009-0008-7987-7134
Bo ZhangDepartment of Oncology, Beijing Shijitan Hospital, Capital Medical University, Beijing 10038, China.
Chenyu LiuDepartment of Oncology, Beijing Shijitan Hospital, Capital Medical University, Beijing 10038, China.
Zubiao NiuAcademy of Military Medical Science, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, Beijing 100071, China.
Yalan YangDepartment of Oncology, Beijing Shijitan Hospital, Capital Medical University, Beijing 10038, China.
You ZhengAcademy of Military Medical Science, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, Beijing 100071, China.
Zhuoran SunAcademy of Military Medical Science, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, Beijing 100071, China.ORCID 0009-0006-4270-5924
Ying ZhangDepartment of Oncology, Beijing Shijitan Hospital, Capital Medical University, Beijing 10038, China.ORCID 0000-0001-8070-6449
Shinan ZhangDepartment of Oncology, Beijing Shijitan Hospital, Capital Medical University, Beijing 10038, China.
Gerry MelinoDepartment of Experimental Medicine, TOR, University of Rome "Tor Vergata", Rome 00133, Italy.ORCID 0000-0001-9428-5972
Hongyan HuangDepartment of Oncology, Beijing Shijitan Hospital, Capital Medical University, Beijing 10038, China.ORCID 0000-0001-8340-6660
Qiang SunAcademy of Military Medical Science, Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, Beijing 100071, China.ORCID 0000-0002-5342-0637

Funding

cams innovation fund for medical sciences 2021-I2M-5-008chinese postdoctoral science foundation 2023MF723196MOST | National Key Research and Development Program of China (NKPs) 2022YFA0912400MOST | National Key Research and Development Program of China (NKPs) 2023YFA0914900MOST | National Natural Science Foundation of China (NSFC) 32450119MOST | National Natural Science Foundation of China (NSFC) 82273184postdoctoral fellowship program of CPSF GZB20240992
6 · The paper itself

Abstract

Despite great success in certain cancers, immunotherapy made little progress in treating immune cold tumors, largely attributed to an immune-suppressive tumor microenvironment with elusive mechanisms. Here, we report in prostate cancer cells a positive feedback loop driven by phosphoserine aminotransferase 1 (PSAT1) that could be targeted to render effective cytotherapy by natural killer (NK) cells. In the loop, PSAT1 increases Y-box binding protein 1 (YBX1) phosphorylation by microtubule affinity-regulating kinase 2, promoting its nuclear translocation to upregulate PSAT1 transcription. Meanwhile, YBX1 also promotes human leukocyte antigens E (HLA-E) transcription to inactivate NK cells. Consequently, the PSAT1 loop serves as a buff sustaining YBX1/HLA-E expression, suppressing NK killing of prostate cancer cells. Targeting loop molecules, such as PAST1, effectively potentiates tumor suppression by NK cells both in-vitro and in-vivo. Thus, our study uncovered a heretofore unrecognized nonautonomous mechanism for PSAT1, as well as a molecular buff for YBX1, to drive tumor growth by evading NK immunity, providing a promising target for NK cytotherapy of immune cold tumors.

Indexed as

Histocompatibility Antigens Class IKiller Cells, NaturalProstatic NeoplasmsY-Box-Binding Protein 1AnimalsCell Line, TumorHumansMaleMicePhosphorylationTranscription, GeneticTumor MicroenvironmentHistocompatibility Antigens Class IY-Box-Binding Protein 1YBX1 protein, humanHLA-EimmunotherapyNK immunityprostate cancerPSAT1

Identifiers

PMID41428871
PMCPMC12772220

What Socratic 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 Socratic graph.