ArticleDiscover oncology2025
P4HA1 is highly expressed in gastric cancer and promotes proliferation and metastasis of gastric cancer cells.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Cadonilimab plus chemotherapy for patients with HER2-negative advanced gastric or gastroesophageal junction adenocarcinoma in China and the United States: a cost-effectiveness analysis.Therapeutic advances in medical 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
7 authors.
Funding
Abstract
backgroundGastric cancer (GC), a prevalent aggressive form of tumor, imposes a significant burden in terms of morbidity and mortality. Prolyl 4-hydroxylase, alpha polypeptide I (P4HA1), a key enzyme in collagen synthesis, comprises two identical alpha subunits and two beta subunits. Studies on the expression and impact of P4HA1 in GC cells are limited.
methodsThe expression and prognosis of P4HA1 in GC were analyzed using bioinformatics. To confirm the P4HA1 level in GC tissues and cells, Western blot (WB) and RT-qPCR experiments were conducted. The signaling pathways related to P4HA1 in GC were examined using the DAVID database. Moreover, the expression of P4HA1 was downregulated by transfecting GC cell lines (HGC-27 and SGC-7901) with siRNA technology. Furthermore, GC proliferation, migration, and invasion were detected via plate cloning, CCK-8, and Transwell assays. The epithelial-mesenchymal transition (EMT) genes (E-cadherin, N-cadherin, Vimentin) and the stemness marker CD44 protein expression in GC cells were detected using WB. The sphere-forming ability of GC cells was analyzed using a sphere-forming assay to determine the effect of P4HA1.
resultsBioinformatics and experimental analyses demonstrated that P4HA1 expression was extensively detected in GC tissues and cells, and strongly related to a poor prognosis for GC. In vitro studies demonstrated that P4HA1 suppression hindered the proliferation, migration, and invasion of GC cells and suppressed EMT characteristics. Both sphere-forming and WB assays revealed that the sphere-forming potential of GC cells and the level of CD44 protein decreased after knocking down the expression of P4HA1, indicating that suppression of P4HA1 could inhibit the stemness of GC cells.
conclusionThe study concluded that P4HA1 has the potential to be expressed substantially in GC tissues and cells and is capable of enhancing the proliferation, metastasis, and stemness of GC.
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.