ArticleFrontiers in cell and developmental biology2026
DNMT3B- SLC25A6 axis-mediated DNA methylation regulates ferroptosis to promote paclitaxel resistance in triple-negative breast cancer.
Article in Frontiers in cell and developmental biology, 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Triple negative breast cancer (TNBC) is the most malignant type of breast cancer, and its treatment usually uses paclitaxel for chemotherapy. However, TNBC cells are increasingly resistant to paclitaxel. In the context of paclitaxel resistance, we investigated the role of DNA methylation and the DNA methyltransferase DNMT3B methylation regulatory proteins, as well as their interaction with ferroptosis regulator SLC25A6, in regulating paclitaxel resistance and ferroptosis in TNBC. Methods: We used database integration analysis methods, combined with bioinformatics screening, Results: DNMT3B was significantly overexpressed in paclitaxel-resistant TNBC tissues and cell lines, correlating with enhanced proliferation, migration, and ferroptosis. Mechanistically, DNMT3B induced DNA methylation of SLC25A6 through its 252-bp CpG island, inhibited its protein expression, and triggered ferroptosis by disrupting mitochondrial function and redox balance, leading to paclitaxel resistance in TNBC. Conclusion: In paclitaxel-resistant TNBC, DNMT3B regulates SLC25A6 expression via DNA methylation, and the DNMT3B-SLC25A6 regulatory axis acts as a central regulator of ferroptosis, promoting paclitaxel resistance in TNBC by suppressing ferroptosis via oxidative stress imbalance. These findings provide promising therapeutic targets for the intervention of TNBC paclitaxel resistance.
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.