ArticleScientific reports2025
Silencing of PIGU inhibits the progression of esophageal squamous cell carcinoma through the PI3K/AKT signaling pathway.
Article in Scientific reports, 2025. 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
12 authors.
Funding
Abstract
Phosphatidylinositol glycan anchor biosynthesis class U (PIGU), a crucial subunit of the glycosylphosphatidylinositol transamidase (GPI-T) complex, is an oncogene in hepatocellular carcinoma. However, its role in esophageal squamous cell carcinoma (ESCC) remains poorly understood. This study aims to clarify PIGU's role and mechanisms in ESCC by analyzing its expression across pan-cancer datasets, clinical relevance in TCGA-ESCA samples, and effects on cell behavior (migration, invasion, proliferation) and signaling pathways, validated via immunohistochemistry. To examine cell behavior, we used Transwell, colony-formation, CCK-8, and wound-healing assays to assess migration, invasion, proliferation, and wound healing.The epithelial-mesenchymal transition marker levels were measured using Western blot analysis, and the cell cycle and apoptosis were assessed using flow cytometry in conjunction with western blotting. Furthermore, we used western blotting to examine proteins implicated in the PI3K/AKT signaling pathway.To further confirm PIGU's role in ESCC progression, a subcutaneous xenograft mouse model was employed. Our findings suggest that PIGU is highly expressed in ESCC and is strongly associated with tumor growth, lymphatic metastasis and poor prognosis, and is an independent prognostic factor for ESCC patients.PIGU knockdown not only arrested the cell cycle and induced apoptosis, but also significantly reduced migration, invasion, and proliferation in ESCC cells. Additionally, vimentin and N-cadherin were downregulated when PIGU expression was silenced, although E-cadherin expression was simultaneously increased.Moreover, PIGU knockdown decreased the amount of phosphorylated Akt and PI3K. In vivo, PIGU knockdown inhibited ESCC cell proliferation and promoted apoptosis. These findings imply that targeting PIGU may represent a promising therapeutic approach, and that PIGU could potentially serve as both a diagnostic and prognostic biomarker for esophageal squamous cell carcinoma (ESCC).
Indexed as
Identifiers
What 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.