ArticleCell adhesion & migration2026
RBM15B-mediated m6A modification of FOXM1 activates the AURKA/TPX2 axis to promote epithelial-mesenchymal transition-driven endometrial cancer progression.
Article in Cell adhesion & migration, 2026. 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometrial cancer(EC) is increasing worldwide, but its molecular mechanisms remain unclear. This study explored whether RBM15B-mediated m6A modification of FOXM1 promotes EC progression through the AURKA/TPX2 axis and epithelial-mesenchymal transition(EMT). Bioinformatics analyses assessed FOXM1 expression and prognosis in EC. RNA pull-down, MeRIP-PCR, dot blot, and RNA stability assays examined m6A regulation. Colony formation, Transwell, wound healing, and tumor sphere assays evaluated malignant behaviors. FOXM1 was significantly upregulated in EC and associated with unfavorable prognosis. Functional assays showed that FOXM1 enhanced proliferation, migration, invasion, and stemness of EC cells. Mechanistically, RBM15B increased m6A modification of FOXM1 mRNA and promoted expression. RBM15B knockdown inhibited malignant phenotypes and reduced activation of the downstream AURKA/TPX2 pathway. RBM15B-mediated m6A methylation stabilizes FOXM1 expression, activates the AURKA/TPX2 axis, and promotes EMT and EC progression. Targeting the RBM15B/FOXM1/AURKA/TPX2 pathway may offer therapeutic potential.
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.