ArticleThe breast journal2026
Inhibition of miR-301a-3p Expression Promotes Ferroptosis: A New Target for Ferroptosis Treatment in TNBC.
Article in The breast journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Inhibition of miR-301a-3p Expression Promotes Ferroptosis: A New Target for Ferroptosis Treatment in TNBC.The breast journal · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
backgroundThe current treatment of triple-negative breast cancer (TNBC) remains challenging; however, regulating ferroptosis through miRNAs offers new insights for TNBC treatment strategies.
methodsBioinformatics methods were used to screen ferroptosis-related differentially expressed genes (FRDEGs) in TNBC, and ferroptosis-related miRNAs were screened by combining gene-miRNA interaction network, miRNA survival analysis, and expression validation in clinical specimens. A nomogram was constructed to evaluate the prognostic impact of miR-301a-3p in TNBC. Cell proliferation and migration capabilities were assessed using the CCK-8 assay, colony formation assay, and wound healing assay, respectively. The intracellular protein expression of GPX4 was measured by Western blot, and fluorescent probes were used to detect intracellular ROS and Fe
resultsThis study used bioinformatics methods to screen five FRDEGs in TNBC, thereby identifying six core miRNAs that can regulate these genes. Among these, miR-301a-3p expression was significantly upregulated in tumor tissues compared to adjacent normal tissues and was associated with poor patient prognosis. Subsequently, an excellent prediction model was established using miR-301a-3p expression information and patient clinicopathological information. Functional analyses revealed that miR-301a-3p promoted TNBC cell proliferation and migration. In addition, the inhibition of cell proliferation activity by miR-301a-3p inhibitor could be reversed by Ferrostatin-1, and miR-301a-3p inhibitor could inhibit the expression of GPX4 and promote the accumulation of intracellular ROS and Fe
conclusionIn conclusion, this study provides evidence that inhibition of miR-301a-3p expression promotes ferroptosis in TNBC cells and produces a synergistic anti-cancer effect with Erastin, providing a new target for future TNBC ferroptosis treatment strategies.
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