ArticleHuman cell2026
The sialyltransferase ST3GAL1 mediates MUCL1 sialylation to exacerbate breast cancer progression.
Article in Human cell, 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
8 authors.
Funding
Abstract
Breast cancer is highly heterogeneous and involves complex molecular mechanisms, posing significant therapeutic challenges. Glycosylation modifications, particularly sialylation, play a critical role in tumor progression. The sialyltransferase ST3GAL1 is highly expressed in breast cancer, yet its functional interaction with MUCL1 and underlying mechanisms remain elusive. Using in vitro and in vivo models, this study systematically investigated the ST3GAL1-mediated sialylation of MUCL1 and its functional impact on breast cancer progression. The results demonstrated that ST3GAL1 directly binds to MUCL1 and catalyzes its sialylation, thereby increasing MUCL1 protein stability and promoting malignant phenotypes. ST3GAL1 knockdown significantly inhibited cell proliferation, migration, and invasion while inducing apoptosis; its overexpression resulted in the opposite effects. These protumorigenic phenotypes were effectively reversed by treatment with the sialyltransferase inhibitor Lith-O-Asp or MUCL1 knockdown. Moreover, ST3GAL1 knockdown suppressed tumor growth and lung metastasis in vivo. These findings reveal a novel ST3GAL1-MUCL1 regulatory axis that drives breast cancer progression through sialylation, offering a promising target for glycotherapy.
Indexed as
Identifiers
41770470What 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.