ArticleTranslational cancer research2026
PRSS1 promotes gastric cancer invasion and metastasis by induction of the epithelial-mesenchymal transition and activation of the MAPK/ERK pathway.
Article in Translational cancer research, 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
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Protease serine 1 (PRSS1) has been implicated in various pathological processes. This study utilized bioinformatics analyses to evaluate PRSS1 expression in gastric cancer (GC) and explore its role in tumor invasion and metastasis. Methods: GC-related differentially expressed genes were identified using Gene Expression Omnibus (GEO) datasets. A combination of bioinformatics analysis and literature review identified PRSS1 as a hub gene, and its putative functions were inferred by functional enrichment analyses. PRSS1 expression levels were verified in GC tissues, cell lines, and serum samples from patients with metastatic lesions using Western blotting, quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assays (ELISAs), and their association with clinicopathological characteristics was analyzed. A stable PRSS1-knockdown cell line was generated to evaluate the effects of the gene on cell migration and invasion, using wound-healing and Transwell migration/invasion assays, as well as in a mouse model of peritoneal metastasis. Altered expression of epithelial-mesenchymal transition (EMT)-related and MAPK/ERK pathway proteins was examined using Western blotting and immunofluorescence. Results: PRSS1 expression was markedly upregulated in HGC-27 and MKN-45 GC cells relative to that in normal gastric mucosal cells. Serum levels of PRSS1 were significantly elevated in patients with GC, particularly those with advanced-stage disease, and were strongly correlated with unfavorable clinicopathology: vascular invasion, Tumor Node Metastasis (TNM) staging, and lymph node metastasis. Functional enrichment analyses indicated involvement of PRSS1 in multiple biological processes associated with tumor progression. Silencing of PRSS1 suppressed migration and invasion of GC cells Conclusions: These findings indicate that PRSS1 is overexpressed in GC and may contribute to invasion and metastasis, possibly through induction of EMT and activation of MAPK/ERK signaling, highlighting its potential as a therapeutic target.
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.