Loading
Life sciences · Journal article
Frontiers in Cell and Developmental Biology · October 19, 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.
The fibrotic subtype of the tumor microenvironment characterized by epithelial-mesenchymal transition, fibrosis, angiogenesis and immune exclusion, predicts poor outcomes across diverse malignancies, yet the role of miR-145 in this context remains unexplored. Leveraging The Cancer Genome Atlas head and neck squamous cell carcinoma (HNSCC) and breast cancer (BRCA) databases, we demonstrate that miR-145 reprogramming recapitulates a noninflamed fibrotic phenotype with immune exclusion. In high miR-145 tumors, EMT programs persist alongside abundant cancer-associated fibroblasts, matrix remodeling and angiogenesis, with upregulation of NOTCH, TGF-β, myogenesis, hypoxia, Hedgehog, and Wnt/β-catenin signaling and downregulation of interferon-γ and JAK–STAT pathways. Our findings illustrate that cancer–stromal juxtacrine interactions activate NOTCH signaling, forming a positive feedback loop that amplifies miR-145 expression and is reinforced by miR-145 promoter hypomethylation. High miR-145 promotes autophagy and mitochondrial oxidative phosphorylation (OXPHOS) metabolism in cancer cells, with GAPDH serving as a central hub linking metabolism, noninflamed immune modulation, and poor clinical outcomes. In vivo, high miR-145 carcinoma cells co-engrafted with fibroblasts drive tumor growth through enhanced metabolism, angiogenesis and immune evasion. This study establishes miR-145 as a driver and biomarker of the fibrotic tumor microenvironment to better inform future cancer therapy strategies.