ArticleScientific reports2025
RUNX1 promotes proliferation of cervical cancer through TGFB2-MAPK pathway.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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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Who cites it
4 citing papers in PubMed.
- Targeting Runx1 Slows Cyst Growth in Autosomal Dominant Polycystic Kidney Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Recurrent PIK3CA-E545K mutation promotes cervical cancer growth and invasion via AKT/mTOR signaling.Molecular genetics and genomics : MGG · 2026Article
- Disruption of ovarian function and induction of apoptosis in female mice by Brefeldin A: Mechanistic insights into reproductive toxicity.Animal models and experimental medicine · 2025Article
- Let-7c/RUNX1 Axis Promotes Cervical Cancer: A Bioinformatic Analysis.Current issues in molecular biology · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
As cervical cancer (CC) caused more than 300,000 deaths in the world, it is urgent to identify therapeutic targets to improve survival. Though RUNX1 is overexpressed in CC, its specific role and underlying molecular mechanisms remain incompletely understood. Here we presented that RUNX1 was upregulated in CC and associated with poor prognosis. Functional studies demonstrated that RUNX1 acts as an oncogene in CC, with overexpression accelerating cell cycle progression and promoting cell proliferation. Mechanistically, RUNX1 regulates the MAPK pathway by modulating TGFB2 expression, while TGFB2 inhibition impaired MAPK pathway activation and the proliferation driven by RUNX1 overexpression. Comprehensive analyses also suggested that RUNX1 may modulate the immune microenvironment in CC through TGFB2. These findings indicate that RUNX1 promotes CC progression by activating the MAPK pathway through upregulation of TGFB2. Our study provides new insights into the role of RUNX1 in CC proliferation and suggests RUNX1 as a potential therapeutic target in CC.
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