ArticleOncogene2026
Targeting the PRMT5-CBX8 axis overcomes dual barriers of CD8⁺ T cell exclusion and tumor stemness for sensitizing TNBC to anti-PD-1 therapy.
Article in Oncogene, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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.
The trial behind it
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Authors and funding
15 authors.
Funding
Abstract
The efficacy of immune checkpoint blockade in triple-negative breast cancer (TNBC) is limited by poor CD8⁺ T cell infiltration. Here, we demonstrate that tumor-derived proprotein convertase subtilisin/kexin type 9 (PCSK9) drives CD8⁺ T cell exclusion, and we identify protein arginine methyltransferase 5 (PRMT5) as an important epigenetic regulator responsible for PCSK9 expression in TNBC. Mechanistically, we elucidate that PRMT5-mediated methylation of the chromobox homolog 8 (CBX8) facilitates its interaction with the deubiquitinase USP7, which removes K33-linked ubiquitination on CBX8. This post-translational modification modulates CBX8 function, enabling it to drive the transcriptional upregulation of key downstream targets PCSK9, which inhibits CD8
Identifiers
42736388What Socratic holds
Registered trials
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.