View in EDS

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

Saved in:
Bibliographic Details
Title: A PSAT1 buff of YBX1 transcriptionally sustains HLA-E-mediated evasion of NK immunity.
Authors: Zhang, Yangyi1,2,3, Ren, He1,2, Ma, Chaobing1, Shi, Changhong4, Yang, Ruigang2, Wang, Chenxi2, Feng, Pengfei2, Zhang, Bo1,2, Liu, Chenyu1, Niu, Zubiao2, Yang, Yalan1, Zheng, You2, Sun, Zhuoran2, Zhang, Ying1, Zhang, Shinan1, Melino, Gerry5, Huang, Hongyan1,3 hhongy1999@126.com, Sun, Qiang2 sunq@bmi.ac.cn
Source: Proceedings of the National Academy of Sciences of the United States of America. 2025, Vol. 122 Issue 52, p1-11. 11p.
Subjects: Killer cells, Immunotherapy, Tumor microenvironment, Prostate cancer, Histocompatibility class I antigens, Genes
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. [ABSTRACT FROM AUTHOR]
Copyright of Proceedings of the National Academy of Sciences of the United States of America is the property of National Academy of Sciences and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Engineering Source
FullText Text:
  Availability: 0
Header DbId: egs
DbLabel: Engineering Source
An: 190780347
AccessLevel: 6
PubType: Academic Journal
PubTypeId: academicJournal
PreciseRelevancyScore: 0
IllustrationInfo
Items – Name: Title
  Label: Title
  Group: Ti
  Data: A PSAT1 buff of YBX1 transcriptionally sustains HLA-E-mediated evasion of NK immunity.
– Name: Author
  Label: Authors
  Group: Au
  Data: <searchLink fieldCode="AR" term="%22Zhang%2C+Yangyi%22">Zhang, Yangyi</searchLink><relatesTo>1,2,3</relatesTo><br /><searchLink fieldCode="AR" term="%22Ren%2C+He%22">Ren, He</searchLink><relatesTo>1,2</relatesTo><br /><searchLink fieldCode="AR" term="%22Ma%2C+Chaobing%22">Ma, Chaobing</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Shi%2C+Changhong%22">Shi, Changhong</searchLink><relatesTo>4</relatesTo><br /><searchLink fieldCode="AR" term="%22Yang%2C+Ruigang%22">Yang, Ruigang</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Wang%2C+Chenxi%22">Wang, Chenxi</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Feng%2C+Pengfei%22">Feng, Pengfei</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Zhang%2C+Bo%22">Zhang, Bo</searchLink><relatesTo>1,2</relatesTo><br /><searchLink fieldCode="AR" term="%22Liu%2C+Chenyu%22">Liu, Chenyu</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Niu%2C+Zubiao%22">Niu, Zubiao</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Yang%2C+Yalan%22">Yang, Yalan</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Zheng%2C+You%22">Zheng, You</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Sun%2C+Zhuoran%22">Sun, Zhuoran</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Zhang%2C+Ying%22">Zhang, Ying</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Zhang%2C+Shinan%22">Zhang, Shinan</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Melino%2C+Gerry%22">Melino, Gerry</searchLink><relatesTo>5</relatesTo><br /><searchLink fieldCode="AR" term="%22Huang%2C+Hongyan%22">Huang, Hongyan</searchLink><relatesTo>1,3</relatesTo><i> hhongy1999@126.com</i><br /><searchLink fieldCode="AR" term="%22Sun%2C+Qiang%22">Sun, Qiang</searchLink><relatesTo>2</relatesTo><i> sunq@bmi.ac.cn</i>
– Name: TitleSource
  Label: Source
  Group: Src
  Data: <searchLink fieldCode="JN" term="%22Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America%22">Proceedings of the National Academy of Sciences of the United States of America</searchLink>. 2025, Vol. 122 Issue 52, p1-11. 11p.
– Name: Subject
  Label: Subjects
  Group: Su
  Data: <searchLink fieldCode="DE" term="%22Killer+cells%22">Killer cells</searchLink><br /><searchLink fieldCode="DE" term="%22Immunotherapy%22">Immunotherapy</searchLink><br /><searchLink fieldCode="DE" term="%22Tumor+microenvironment%22">Tumor microenvironment</searchLink><br /><searchLink fieldCode="DE" term="%22Prostate+cancer%22">Prostate cancer</searchLink><br /><searchLink fieldCode="DE" term="%22Histocompatibility+class+I+antigens%22">Histocompatibility class I antigens</searchLink><br /><searchLink fieldCode="DE" term="%22Genes%22">Genes</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: 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. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of Proceedings of the National Academy of Sciences of the United States of America is the property of National Academy of Sciences and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
PLink https://search.ebscohost.com/login.aspx?direct=true&site=eds-live&db=egs&AN=190780347
RecordInfo BibRecord:
  BibEntity:
    Identifiers:
      – Type: doi
        Value: 10.1073/pnas.2505658122
    Languages:
      – Code: eng
        Text: English
    PhysicalDescription:
      Pagination:
        PageCount: 11
        StartPage: 1
    Subjects:
      – SubjectFull: Killer cells
        Type: general
      – SubjectFull: Immunotherapy
        Type: general
      – SubjectFull: Tumor microenvironment
        Type: general
      – SubjectFull: Prostate cancer
        Type: general
      – SubjectFull: Histocompatibility class I antigens
        Type: general
      – SubjectFull: Genes
        Type: general
    Titles:
      – TitleFull: A PSAT1 buff of YBX1 transcriptionally sustains HLA-E-mediated evasion of NK immunity.
        Type: main
  BibRelationships:
    HasContributorRelationships:
      – PersonEntity:
          Name:
            NameFull: Zhang, Yangyi
      – PersonEntity:
          Name:
            NameFull: Ren, He
      – PersonEntity:
          Name:
            NameFull: Ma, Chaobing
      – PersonEntity:
          Name:
            NameFull: Shi, Changhong
      – PersonEntity:
          Name:
            NameFull: Yang, Ruigang
      – PersonEntity:
          Name:
            NameFull: Wang, Chenxi
      – PersonEntity:
          Name:
            NameFull: Feng, Pengfei
      – PersonEntity:
          Name:
            NameFull: Zhang, Bo
      – PersonEntity:
          Name:
            NameFull: Liu, Chenyu
      – PersonEntity:
          Name:
            NameFull: Niu, Zubiao
      – PersonEntity:
          Name:
            NameFull: Yang, Yalan
      – PersonEntity:
          Name:
            NameFull: Zheng, You
      – PersonEntity:
          Name:
            NameFull: Sun, Zhuoran
      – PersonEntity:
          Name:
            NameFull: Zhang, Ying
      – PersonEntity:
          Name:
            NameFull: Zhang, Shinan
      – PersonEntity:
          Name:
            NameFull: Melino, Gerry
      – PersonEntity:
          Name:
            NameFull: Huang, Hongyan
      – PersonEntity:
          Name:
            NameFull: Sun, Qiang
    IsPartOfRelationships:
      – BibEntity:
          Dates:
            – D: 30
              M: 12
              Text: 2025
              Type: published
              Y: 2025
          Identifiers:
            – Type: issn-print
              Value: 00278424
          Numbering:
            – Type: volume
              Value: 122
            – Type: issue
              Value: 52
          Titles:
            – TitleFull: Proceedings of the National Academy of Sciences of the United States of America
              Type: main
ResultId 1