ArticleMolecular pharmacology2025
Heterogeneous nuclear ribonucleoprotein A/B drives gastric cancer and epithelial-mesenchymal transition via the Akt-GSK3β-Wnt pathway.
Article in Molecular pharmacology, 2025. 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer (GC) is a leading cause of cancer-related deaths globally, with metastasis critically impacting prognosis. Splicing factors are key regulators of tumorigenesis, particularly in metastasis. In this exploratory study, we investigated the role and mechanism of heterogeneous nuclear ribonucleoprotein A/B (HNRNPAB) in GC cell invasion and migration. We detected a 3.45-fold increase in HNRNPAB protein levels in highly metastatic MKN45 cells compared with low metastatic MKN7 cells (P < .01) and marked upregulation in human GC tissues (n = 408) versus normal tissues (n = 211, P < .05, predicted by gene expression profiling interactive analysis). HNRNPAB overexpression in MKN45 and MKN7 cells substantially enhanced proliferation by 50% (P < .001, 3-[4,5-dimethyl-2-thiazolyl]-2,5-diphenyl-2-H-tetrazolium bromide assay), migration by 60% (P < .001, wound healing assay), and invasion by 70% (P < .001, Transwell assay), whereas knockdown reduced these by similar magnitudes. Mechanistically, HNRNPAB decreased E-cadherin (0.5 ± 0.1-fold, P < .001) and increased N-cadherin (1.8 ± 0.2-fold), Vimentin (2.0 ± 0.2-fold), and Snail levels (1.7 ± 0.2-fold, P < .001), promoting epithelial-mesenchymal transition, which was associated with Akt-GSK3β-Wnt pathway modulation by elevating phosphorylated Akt (Ser473, 2.0 ± 0.2-fold) and phosphorylated glycogen synthase kinase 3β (Ser9, 1.8 ± 0.2-fold, P < .001). These findings suggest that HNRNPAB is a potential diagnostic and therapeutic target for GC. SIGNIFICANCE STATEMENT: This exploratory study reveals that heterogeneous nuclear ribonucleoprotein A/B is associated with gastric cancer progression and epithelial-mesenchymal transition through its potential modulation of the Akt-GSK3β-Wnt signaling pathway. Targeting heterogeneous nuclear ribonucleoprotein A/B could offer novel therapeutic approaches for improving treatment outcomes in gastric cancer, highlighting its potential as a biomarker for disease prognosis.
Indexed as
Identifiers
What Socratic 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 Socratic graph.