ArticleOncogene2026
ESRP1-regulated DNMT3B isoform switching determines the malignant potential of pancreatic cancer.
Article in Oncogene, 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
23 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial splicing regulatory protein 1 (ESRP1) is a key regulator of epithelial-mesenchymal transition (EMT) and cancer progression, including in pancreatic ductal adenocarcinoma (PDAC). We show that ESRP1-mediated isoform switching of DNA methyltransferase 3B (DNMT3B) correlates with the metastatic potential of pancreatic cancer cells. The expression of DNMT3B splicing variants was closely linked to ESRP1 level. Ectopic expression of mesenchymal DNMT3B isoforms 3 and 7, lacking part of the methyltransferase catalytic domain, significantly enhanced lung metastasis and tumor growth, while epithelial DNMT3B isoforms 1 and 2, with an intact catalytic domain, suppressed these effects in mouse models. Differential expression of DNMT3B isoforms also correlated with overall survival in PDAC patients. Deletion of exons 21-22, differentially spliced region between epithelial and mesenchymal isoforms, increased cell proliferation and migration, similar to mesenchymal DNMT3B. RNA sequencing revealed that mesenchymal DNMT3B isoforms 3 and 7 were associated with aggressive tumor phenotypes. Among differentially expressed target genes of DNMT3B isoforms, Fibulin 1 (FBLN1), a key regulator of the tumor microenvironment, regulates cancer cell migration and EMT. Taken together, our results highlight the central role of ESRP1-mediated DNMT3B isoform switching in pancreatic cancer progression and metastasis and suggest that DNMT3B isoforms may serve as potential biomarkers for this disease.
Indexed as
Identifiers
42432326What 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.