Loading
Life sciences · Journal article
Biology Direct · October 9, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Cancer-associated fibroblasts (CAFs) are key stromal components of the tumor microenvironment (TME), but their potential to deliver the tumor-suppressive signals remains unclear. Here, through integrative single-cell and transcriptomic analyses, we identify miR-486-3p, localized to CAFs and consistent with exosomal delivery, as a critical suppressor of bladder cancer (BLCA) progression. miR-486-3p was consistently downregulated in BLCA tissues and correlated with favorable overall survival, while its direct target HER-2 was upregulated and linked to poor prognosis. Mechanistically, miR-486-3p directly bound the 3′-UTR of HER-2 mRNA, and HER-2 reconstitution abrogated the tumor-suppressive effects of miR-486-3p on proliferation, migration, invasion, and apoptosis. Single-cell RNA-seq of 58,982 cells localized HER-2 and related targets exclusively to malignant populations, with a HER-2-high subpopulation exhibiting hyper-proliferative signatures. Computational screening identified zongertinib as a high-affinity HER-2 inhibitor with favorable pharmacokinetics. Clinically, low miR-486-3p or high HER-2 expression predicted immune-cold phenotypes and resistance to PD-1/PD-L1 blockade in immunotherapy cohorts. Collectively, this study uncovers a stromal-epithelial checkpoint in which miR-486-3p, with its expression localized to CAFs and likely delivered via exosomes, suppresses BLCA by targeting the HER-2/MDK-NCL axis, with implications for prognosis, immune evasion, and HER-2-directed therapy.