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.
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.
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Who cites it
3 citing papers in PubMed.
- A P-body-related risk score predicts prognosis and immune microenvironment in lung adenocarcinoma.Translational cancer research · 2026Article
- Y-box binding protein-1 at the crossroads of DNA damage response and tumor immune evasion.JNCI cancer spectrum · 2026Review
- 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 · 2025Article
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Authors and funding
18 authors.
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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.
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