ArticleTranslational cancer research2026
The WT 1-AS/miR-206 axis regulates the proliferation and migration of breast cancer through the cuproptosis related gene
Article in Translational cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- WT1-AS acts as a tumor suppressor in cervical cancer via OSR2-mediated transcriptional activation.Translational cancer research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Breast cancer (BC) remains one of the most harmful malignancies in women, characterized by high heterogeneity, frequent recurrence, and metastasis. The competitive endogenous RNA (ceRNA) mechanism is crucial in tumor biology. While cuproptosis, a novel copper-induced cell death, shows therapeutic promise in BC, its ceRNA-associated regulatory network is largely unknown. This study aimed to identify and characterize a specific ceRNA axis involved in BC progression and to investigate its functional relationship with cuproptosis. Methods: To explore this, we identified a potential ceRNA axis, WT1-AS/miR-206/BCL11A in BC. Its role was investigated using copper ion and reactive oxygen species (ROS) assays to evaluate cuproptosis, functional enrichment and phenotypic analyses to assess cell proliferation and migration, and luciferase reporter assays to validate molecular interactions. Rescue experiments were further conducted to delineate functional dependencies. Results: We demonstrated that the WT1-AS/miR-206/BCL11A axis promotes BC malignancy. Suppressing BCL11A significantly increased intracellular copper levels and ROS, thereby enhancing cuproptosis. This axis was essential for driving BC cell proliferation and migration. Mechanistically, luciferase assays confirmed that the long non-coding RNA WT1-AS acts as a molecular sponge for miR-206, which in turn targets and upregulates BCL11A expression. Rescue experiments indicated that the oncogenic effects of WT1-AS are partially mediated through BCL11A. Conclusions: Our study elucidates a novel ceRNA network, the WT1-AS/miR-206/BCL11A axis, which regulates BC progression and modulates cuproptosis. These findings provide fresh insights into BC biology and highlight potential diagnostic and therapeutic targets centered on cuproptosis regulation.
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.