ArticleScientific reports2025
The downregulation of ubiquitin-specific peptidase 2 indicates a poor prognosis and promotes the progression of gastric cancer through focal adhesion and ECM pathway signaling.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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.
- Ubiquitin-Specific Protease 2 (USP2) as a Modulator of Energy Metabolism: A Review of Studies Using Animal and Cellular Models.Biomedicines · 2026Review
- The UBE2/E2 ubiquitin-conjugating enzyme family at the interface of tumor biology and antitumor immunity: mechanisms, biomarkers, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors.
Funding
Abstract
Gastric cancer ranks among the most prevalent forms of cancer worldwide. Recent rapid advancements in diagnostic methods, neoadjuvant or adjuvant therapies, and surgical procedures have significantly improved survival rates for patients with gastric cancer. Nonetheless, these benefits have not yet reached the majority of individuals affected. Previous research has indicated that USP2, a component of the ubiquitin system, plays a crucial role in reshaping the proteome and enhancing the prognosis of diseases. However, the current understanding of USP2 expression and the associated pathways in gastric cancer remains unclear. The differential expression of USP2 was examined in pan-cancer, with a particular focus on its expression in gastric cancer cells and patients. Additionally, the impact of USP2 on the proliferation, migration, and apoptosis of gastric cancer cells was explored via CCK8, transwell, and invasion assays. RNA sequencing was employed to investigate pathways associated with USP2, and RT-qPCR and western blotting were utilized to confirm the expression of related pathway genes and proteins. The prognostic value of a model derived from USP2 expression was assessed and validated. USP2 expression was significantly reduced in gastric cancer cells and patient samples (p < 0.05). Patients with low USP2 expression are primarily associated with genetic variations, neoantigen loads, microsatellite instability (MSI) scores, and immune cell infiltration (p < 0.05). The overexpression of USP2 suppresses proliferation, migration, and cell cycle progression while enhancing apoptosis in GC cells. Concurrently, we identified 865 genes whose expression was downregulated. KEGG and GSEA enrichment analyses revealed significant suppression of the focal adhesion and ECM receptor interaction pathways following USP2 overexpression. A genomic model derived from USP2 was constructed and validated for its reliability in predicting patient prognosis. The expression of USP2 was positively correlated with sensitivity to small-molecule drugs, including entinostat, SB590885, and PF-562,271. USP2 acts as a negative regulator of gastric cancer progression. Consequently, USP2 has the potential to be utilized as a therapeutic target to improve the clinical prognosis and survival rates of patients.
Indexed as
Identifiers
What 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.