ArticleCytoJournal2025
Emerging regulators of gastric cancer angiogenesis: Synergistic effects of regulator of G protein signaling 4 and midkine.
Article in CytoJournal, 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.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Globally, gastric cancer (GC) is among the most prevalent cancers. The development and spread of stomach cancer are significantly influenced by angiogenesis. However, the molecular mechanisms underlying this process remain unclear. This study aimed to investigate the role of the regulator of G protein signaling 4 (RGS4) in GC angiogenesis and its potential mechanisms. Material and Methods: Through Results: Our findings revealed that RGS4 is a crucial factor in GC metastasis, significantly inducing angiogenesis. Further studies indicated that RGS4 directly interacts with MDK and upregulates its expression. By upregulating MDK, RGS4 stimulates the angiogenesis and metastasis of GC. Furthermore, a poor prognosis for patients with GC is directly linked to high expression of RGS4 and MDK. Conclusion: This work is the first to clarify the molecular mechanism by which RGS4 upregulates MDK expression to increase GC angiogenesis. These findings not only enhance our understanding of the mechanisms underlying GC progression but also provide potential targets for developing new anti-angiogenic and antimetastatic therapies. RGS4 and MDK could serve as effective biomarkers for predicting the prognosis of patients with GC and offer new insights into personalized treatment approaches.
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.