ArticleScientific reports2025
Regulator of G protein signaling-1 facilitates ovarian cancer development by modulating NF-kB signal pathway.
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 4 papers, 1 of them a synthesis that pooled it.
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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.
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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.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- RGS Family Remodeling in Breast Cancer: A Meta-Analysis and Multi-Omics Profiling of Prognostic Biomarkers.Cancer medicine · 2026Pooled it
- Expression and prognostic diagnostic significance of RGS gene family in breast cancer.Discover oncology · 2025Article
- RGS1 induces nasal epithelial barrier dysfunction in allergic rhinitis by modulating NF-κB/AQP5 axis.Cytotechnology · 2025Article
- The role of macrophage polarization in ovarian cancer: from molecular mechanism to therapeutic potentials.Frontiers in immunology · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
Abstract
Regulator of G protein signaling 1 (RGS1) is known to be highly expressed in various tumors, but its specific effects and regulatory mechanism in ovarian cancer (OC) progression are not well understood. To delve into the tumor biology, a predictive risk model for OC was developed, incorporating RGS1, PRKG2, CD24, and ABCB1, with RGS1 exhibiting the strongest correlation. The model's reliability and validity were confirmed through Kaplan-Meier analysis, receiver operating characteristic (ROC) curve, and principal component analysis (PCA). The risk score was validated as an independent indicator of overall survival, and a nomogram model was created to predict overall survival. Moreover, RGS1 expression was found to be up-regulated and associated with a poor prognosis in OC. Functional studies revealed that deleting RGS1 inhibited OC cell proliferation both in vitro and in vivo, while overexpression of RGS1 enhanced cell proliferation. Additionally, blocking the NF-kB pathway was shown to impede RGS1-induced proliferation, and overexpression of p65 partially reversed the effects of RGS1 deletion, promoting the tumorigenic properties of OC cells. These findings suggest that RGS1 could be a valuable biomarker for predicting prognosis and a potential novel therapeutic target for OC treatment.
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