ArticleDiscover oncology2026
Exosomal miR-4443 confers cisplatin resistance in breast cancer by inhibiting ferroptosis.
Article in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveExosomal microRNAs (miRNAs) have emerged as important regulators of chemotherapy response. This study aimed to investigate whether exosomal miR-4443 is associated with cisplatin resistance in breast cancer and to explore its potential relationship with ferroptosis.
methodsExosomes were isolated from cisplatin-sensitive and cisplatin-resistant breast cancer tissues, as well as from cisplatin-sensitive (MCF-7-S) and cisplatin-resistant (MCF-7-R) breast cancer cell lines. Exosomes were characterized by transmission electron microscopy, nanoparticle tracking analysis, and detection of canonical exosomal markers. miR-4443 expression was quantified by qRT-PCR. Cell viability, colony formation, iron accumulation, and reactive oxygen species (ROS) levels were assessed following cisplatin treatment and modulation of miR-4443 expression. Ferroptosis-related responses were evaluated using pharmacological inducers and inhibitors. The effects of miR-4443 on cisplatin response were further examined in a subcutaneous xenograft model.
resultsExosomal miR-4443 levels were significantly higher in cisplatin-resistant breast cancer tissues and cell lines compared with cisplatin-sensitive counterparts. Exosomes derived from cisplatin-resistant samples transferred miR-4443 to sensitive cells and attenuated cisplatin-induced growth inhibition. Modulation of miR-4443 expression altered cellular sensitivity to cisplatin and ferroptosis-related stress, accompanied by changes in iron accumulation, ROS levels, and expression of the ferroptosis suppressor FSP1. In vivo, miR-4443 overexpression reduced the antitumor efficacy of cisplatin and was associated with increased FSP1 expression in tumor tissues.
conclusionThese findings suggest that exosomal miR-4443 is associated with cisplatin resistance in breast cancer and may contribute to this phenotype, at least in part, through modulation of ferroptosis-related pathways. Targeting miR-4443 or modulating ferroptosis-related pathways may represent a promising strategy to enhance cisplatin sensitivity; however, further mechanistic dissection and larger-scale clinical validation will be required before translational application.
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