ArticleOncogene2025
PSME3 drives Tregs infiltration and anti-PD1 resistance in hepatocellular carcinoma by regulating FBXL7/PTEN-mediated metabolic reprogramming.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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.
Who cites it
3 citing papers in PubMed.
- AI-integrated single-cell multi-omics decodes the hepatocellular carcinoma metabolism-immune axis: a new strategy for precision therapeutic targeting.Frontiers in oncology · 2026Review
- Immunosuppressive cells as barriers to cancer therapy: mechanisms and emerging solutions.Frontiers in immunology · 2026Review
- Noninvasive assessment of core metastatic genes in lung adenocarcinoma: development of a predictive model integrating single-cell transcriptomics and radiomics.Frontiers in oncology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Regulatory T cells (Tregs) contribute to the immune escape of hepatocellular carcinoma (HCC). However, the drivers of the accelerated Treg accumulation in HCC remain unclear. In this study, Treg infiltration-related genes were analysed, and proteasome activator subunit 3 (PSME3) was identified as a pivotal driver using bioinformatics analysis. Functional experiments were performed to investigate the correlation between PSME3 expression and programmed cell death-1 (PD-1) monoclonal antibody therapy resistance in HCC. Elevated levels of PSME3 lead to metabolic reprogramming towards glycolysis and upregulation of osteopontin (OPN) expression. This glycolysis-induced OPN secretion by HCC cells promotes the differentiation and enrichment of Tregs while inhibiting CD8
Indexed as
Identifiers
41094239What OpenQuestion 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 OpenQuestion graph.